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Infertility is a significant cause of anxiety, depression, and social stigma among couples and families. In such cases, male reproductive factors contribute widely to the extent of 20-70%. Male infertility is a multifactorial disease with several complications contributing to its diagnosis. Although its management encompasses both modern and traditional medicine arenas, the first line of treatment, adopted by most males, focuses on the reasonably successful medicinal plant-based conventional therapies. Phyto-therapeutics, which relies on active ingredients from traditionally known herbs, influences sexual behavior and male fertility factors. The potency of these phyto-actives depends on their preparation methods and forms of consumption, including decoctions, extracts, semi-purified compounds, etc., as inferred from in vitro and in vivo (laboratory animal models and human) studies. The mechanisms of action therein involve the testosterone pathway for stimulation of spermatogenesis, reduction of oxidative stress, inhibition of inflammation, activation of signaling pathways in the testes [extracellular-regulated kinase (ERK)/protein kinase B(PKB)/transformation of growth factor-beta 1(TGF-β1)/nuclear factor kappa-light-chain-enhancer of activated B cells NF-kB signaling pathways] and mediation of sexual behavior. This review critically focuses on the medicinal plants and their potent actives, along with the biochemical and molecular mechanisms that modulate vital pathways associated with the successful management of male infertility. Such intrinsic knowledge will significantly further studies on medicinal plants that improve male reproductive health.

Arsenic is one of the heavy metals found in the environment and it is widely spread on the earth. This is due to the industrial and agricultural sectors and acts as an anthropogenic substance. This...

In addition to the COVID-19 waves, the globe is facing global monkeypox (MPX) outbreak. MPX is an uncommon zoonotic infection characterized by symptoms similar to smallpox. It is caused by the monkeypox virus (MPXV), a double-stranded DNA virus that belongs to the genus Orthopoxvirus (OPXV). MPXV, which causes human disease, has been confined to Africa for many years, with only a few isolated cases in other areas. Outside of Africa, the continuing MPXV outbreak in multiple countries in 2022 is the greatest in recorded history. The current outbreak, with over 10 000 confirmed cases in over 50 countries between May and July 2022, demonstrates that MPXV may travel rapidly among humans and pose a danger to human health worldwide. The rapid spread of such outbreaks in recent times has elevated MPX to the status of a rising zoonotic disease with significant epidemic potential. While the MPXV is not as deadly or contagious as the variola virus that causes smallpox, it poses a threat because it could evolve into a more potent human pathogen. This review assesses the potential threat to the human population and provides a brief overview of what is currently known about this reemerging virus. By analyzing the biological effects of MPXV on human health, its shifting epidemiological footprint, and currently available therapeutic options, this review has presented the most recent insights into the biology of the virus. This study also clarifies the key potential causes that could be to blame for the present MPX outbreak and draw attention to major research questions and promising new avenues for combating the current MPX epidemic.

Placental complication arises due to various risk factors occurring during the pregnancy period, leading to an increased morbidity rate. Placenta related disorders are one of primary reason for pregnancy related complications and the clinical incidences are seen to be on the rise. Most of the common disorders associated with placenta are pre-eclampsia, recurrent spontaneous abortions, intra-uterine growth restriction etc. Several studies have been done to understand the genetics and immunological attributes leading to the development of placenta associated complications. In the recent years, studies were able to establish and identify ncRNAs found specifically in foetal tissues such as the placenta. The aberrant expression patterns of ncRNA associated with placenta has been linked to disorders such as pre-eclampsia. Since ncRNA play a major role in regulating biological processes like trophoblast growth, migration and invasion, their aberrant expression could very well lead to complications like spontaneous pregnancy loss. This review article focuses on the association of ncRNAs - miRNAs, lncRNAs, CircRNAs in placenta associated complications as well as the different ncRNA based therapies. Deciphering the exact mechanism involved in the regulation and development of placenta through ncRNA will help in using it as a biomarker for early diagnosis. Understanding the therapeutic opportunities of ncRNAs in placental disorders will result in better treatment strategies.

Research on polycystic ovarian syndrome (PCOS) remains intense due to its evolving impact on metabolism, reproduction and cardiovascular function. Changes in metabolic pathways can also significantly impact renal function including the development of Focal Segmental Glomerulosclerosis (FSGS), one of the most highly investigated renal diseases. In FSGS, scarring of the glomerulus vascular tuft damages the kidneys. Onset of FSGS may either be congenital or due to other disorders that affect the metabolism and normal kidney function. Both PCOS and FSGS appear to be associated with Transforming Growth Factor-β (TGF-β) signalling. Over-expression of TGF-β may be due to the activation of the thrombospondin 1 (TSP1) gene, which increases the probability of developing renal disorders. Higher androgen levels in PCOS may also cause podocyte damage thus directly impacting development of FSGS. This article reviews the role of TGF-β's in PCOS and FSGS and explores the inter-relationship between these two disorders.

This review gives concise information on green technology (GT) and Industrial Revolution 4.0 (IR 4.0). Climate change has begun showing its impacts on the environment, and the change is real. The devastating COVID-19 pandemic has negatively affected lives and the world from the deadly consequences at a social, economic, and environmental level. In order to balance this crisis, there is a need to transition toward green, sustainable forms of living and practices. We need green innovative technologies (GTI) and Internet of Things (IoT) technologies to develop green, durable, biodegradable, and eco-friendly products for a sustainable future. GTI encompasses all innovations that contribute to developing significant products, services, or processes that lower environmental harm, impact, and worsening while augmenting natural resource utilization. Sensors are typically used in IoT environmental monitoring applications to aid ecological safety by nursing air or water quality, atmospheric or soil conditions, and even monitoring species' movements and habitats. The industries and the governments are working together, have come up with solutions-the Green New Deal, carbon pricing, use of bio-based products as biopesticides, in biopharmaceuticals, green building materials, bio-based membrane filters for removing pollutants, bioenergy, biofuels and are essential for the green recovery of world economies. Environmental biotechnology, Green Chemical Engineering, more bio-based materials to separate pollutants, and product engineering of advanced materials and environmental economies are discussed here to pave the way toward the Sustainable Development Goals (SDGs) set by the UN and achieve the much-needed IR 4.0 for a greener-balanced environment and a sustainable future.

Microplastics (MPs) have become a significant source of concern as they have emerged as a widespread pollutant that harms the aquatic environment. It has become an enormous challenge, having the capacity to biomagnify and eventually affect human health, biodiversity, aquatic animals, and the environment. This review provides in-depth knowledge of how MPs interact with different toxic organic chemicals, antibiotics, and heavy metals in the aquatic environment and its consequences. Membrane technologies like ultrafiltration (UF), nanofiltration (NF), microfiltration (MF), and dynamic membranes can be highly effective techniques for the removal of MPs. Also, hybrid membrane techniques like advanced oxidation processes (AOPs), membrane fouling, electrochemical processes, and adsorption processes can be incorporated for superior efficiency. The review also focuses on the reactor design and performance of several membrane-based filters and bioreactors to develop practical, feasible, and sustainable membrane technologies. The main aim of this work is to throw light on the alarming scenario of microplastic pollution in the aquatic milieu and strategies that can be adopted to tackle it.

In recent years, oncotherapy has received considerable attention concerning plant polyphenols. Increasing evidence suggests that because of the efficiency of polyphenols, they may have anti-tumour effects in various cancers. However, their regulatory structures remain elusive. Long non-coding RNAs (lncRNAs) have been identified in the regulation of various forms of tumorigenesis and tumour development. Long non-coding RNAs have recently emerged as regulatory eukaryotic transcripts and therapeutic targets with important and diverse functions in health and diseases. LncRNAs may be associated with the initiation, development, and progression of cancer. This review summarizes the research on the modulatory effects of IncRNAs and their roles in mediating cellular processes. The mechanisms of action of polyphenols underlying their therapeutic effects on cancers are also discussed. Based on our review, polyphenols might facilitate a significant epigenetic modification as part of their tissue- and/or cell-related biological effects. This finding may be attributed to their interaction with cellular signalling pathways involved in chronic diseases. Certain lncRNAs might be the target of specific polyphenols, and some critical signalling processes involved in the intervention of cancers might mediate the therapeutic roles of polyphenols.

Stroke is one of the main causes of mortality and disability, and it is due to be included in monetary implications on wellbeing frameworks around the world. Ischemic stroke is caused by interference in cerebral blood flow, leading to a deficit in the supply of oxygen to the affected region. It accounts for nearly 80–85% of all cases of stroke. Oxidative stress has a significant impact on the pathophysiologic cascade in brain damage leading to stroke. In the acute phase, oxidative stress mediates severe toxicity, and it initiates and contributes to late-stage apoptosis and inflammation. Oxidative stress conditions occur when the antioxidant defense in the body is unable to counteract the production and aggregation of reactive oxygen species (ROS). The previous literature has shown that phytochemicals and other natural products not only scavenge oxygen free radicals but also improve the expressions of cellular antioxidant enzymes and molecules. Consequently, these products protect against ROS-mediated cellular injury. This review aims to give an overview of the most relevant data reported in the literature on polyphenolic compounds, namely, gallic acid, resveratrol, quercetin, kaempferol, mangiferin, epigallocatechin, and pinocembrin, in terms of their antioxidant effects and potential protective activity against ischemic stroke.

Heavy metal and metalloid poisoning in the environment and food has piqued the public’s interest since it poses significant hazards to the ecological system and human health. In food, several metals, including cadmium (Cd), lead (Pb), mercury (Hg), tin (Sn), manganese (Mn), and aluminium (Al), and metalloids, including arsenic (As), antimony (Sb), and selenium (Se), pose a severe threat to human health. It is of utmost importance to detect even minute quantities of these toxic elements and this must be efficiently determined to understand their risk. Several traditional and advanced technologies, including atomic absorption spectrometry (AAS), spectrofluorimetry, inductively coupled plasma spectrometry, e-tongues, electrochemical aptasensors, Raman spectroscopy, and fluorescence sensors, among other techniques, have proven highly beneficial in quantifying even the minute concentrations of heavy metals and metalloids in food and dietary supplements. Hence, this review aims to understand the toxicity of these metals and metalloids in food and to shed light on the emerging technologies for their detection.

This review provides a detailed study of pancreatic cancer (PC) and the implication of different types of cancers concerning diabetes. The combination of anti-diabetic drugs with other anti-cancer drugs and phytochemicals can help prevent and treat this disease. PC cancer stem cells (CSCs) and how they migrate and develop into malignant tumors are discussed. A detailed explanation of the different mechanisms of diabetes development, which can enhance the pancreatic CSCs' proliferation by increasing the IGF factor levels, epigenetic modifications, DNA damage, and the influence of lifestyle factors like obesity, and inflammation, has been discussed. It also explains how cancer due to diabetes is associated with high mortality rates. One of the well-known diabetic drugs, metformin, can be combined with other anti-cancer drugs and prevent the development of PC and has been taken as one of the prime focus in this review. Overall, this paper provides insight into the relationship between diabetes and PC and the methods that can be employed to diagnose this disease at an earlier stage successfully.

Heavy metals and metalloid exposure are among the most common factors responsible for reproductive toxicity in human beings. Several studies have indicated that numerous metals and metalloids can display severe adverse properties on the human reproductive system. Metals like lead, silver, cadmium, uranium, vanadium, and mercury and metalloids like arsenic have been known to induce reproductive toxicity. Moderate to minute quantities of lead may affect several reproductive parameters and even affect semen quality. The ecological and industrial exposures to the various heavy metals and metalloids have disastrous effects on the reproductive system ensuing in infertility. This work emphasizes the mechanism and pathophysiology of the aforementioned heavy metals and metalloids in reproductive toxicity. Additionally, this work aims to cover the classical protective mechanisms of zinc, melatonin, chelation therapy, and other trending methods to prevent heavy metal-induced reproductive toxicity.

The highly active estrogen metabolism and receptor protein expression are to blame for the elevated breast cancer (BC) rate in post-menopausal women. Letrozole is a powerful endocrine medication that targets and inhibits the aromatase, often known as an aromatase inhibitor (AI). It aids in the adjuvant, neoadjuvant, and metastatic treatment of HR+ breast cancer because it can boost FSH production for ovulation induction. It has recently been used in infertile pre-menopausal women. The main advantages of utilizing letrozole to enhance follicle development may be wasted in current infertility treatments. We went into great length in this review about the pharmacokinetics, pharmacodynamics, and distinct adverse effects of the drug on the heart, kidney, liver, embryo, bone, and ovary. It also causes apoptosis, necrosis, and fibrosis, which all result in the demise of cancer cells. Its central and peripheral effects on follicle formation, estrogen production in the ovaries, and their clinical implications are explored in detail in this work.

Human diseases such as cancer can be caused by aberrant epigenetic regulation. Polyphenols play a major role in mammalian epigenome regulation through mechanisms and proteins that remodel chromatin. In fruits, seeds, and vegetables, as well as food supplements, polyphenols are found. Compounds such as these ones are powerful anticancer agents and antioxidants. Gallic acid, kaempferol, curcumin, quercetin, and resveratrol, among others, have potent anti-tumor effects by helping reverse epigenetic changes associated with oncogene activation and tumor suppressor gene inactivation. The role dietary polyphenols plays in restoring epigenetic alterations in cancer cells with a particular focus on DNA methylation and histone modifications was summarized. We also discussed how these natural compounds modulate gene expression at the epigenetic level and described their molecular targets in cancer. It highlights the potential of polyphenols as an alternative therapeutic approach in cancer since they modulate epigenetic activity.

Cardiotoxicity by anthracycline antineoplastic drug doxorubicin is one of the systemic toxicity of the cardiovascular system. The mechanism responsible for doxorubicin cardiotoxicity and lipid metabolism remains elusive. The current study tested the hypotheses that the role of peroxisome proliferator-activated receptor α (PPARα) in the progress of doxorubicin-induced cardiomyopathy and its mechanism behind lipid metabolism. In the present study, male rats were subjected to intraperitoneal injection (5-week period) of doxorubicin with different dosages such as low dosage (1.5 mg/kg body weight) and high dosage (15 mg/kg body weight) to induce doxorubicin cardiomyopathy. Myocardial PPARα was impaired in both low dosage and high dosage of doxorubicin-treated rats in a dose-dependent manner. The attenuated level of PPARα impairs the expression of the genes involved in mitochondrial transporter, fatty acid transportation, lipolysis, lipid metabolism, and fatty acid oxidation. Moreover, it disturbs the reverse triacylglycerol transporter apolipoprotein B-100 (APOB) in the myocardium. Doxorubicin elevates the circulatory lipid profile and glucose. Further aggravated lipid profile in circulation impedes the metabolism of lipid in cardiac tissue, which causes a lipotoxic condition in the heart and subsequently associated disease for the period of doxorubicin treatment. Elevated lipids in the circulation translocate into the heart dysregulates lipid metabolism in the heart, which causes augmented oxidative stress and necro-apoptosis and mediates lipotoxic conditions. This finding determines the mechanistic role of doxorubicin-disturbed lipid metabolism via PPARα, which leads to cardiac dysfunction.

Fatty liver disease (FLD) is one of the largest burdens to human health worldwide and is associated with gut microbiome and metabolite stability. Engineered liver tissues have shown promise in restoring liver functions in non-alcoholic FLD (NAFLD), hepatitis and cirrhosis. Fatty liver, largely noted in obesity and hepatic cancer, is highly fatal and has led to a global increase in death rates. It is associated with complex metabolic reprogramming too. A standard approach to therapy in the newly diagnosed setting includes surgery or identification of biomarkers/ metabolites for therapeutic purposes, which ultimately focus on improvement of liver health in patients. As such there are no standard procedures for patient care, but depending on the severity, systemic therapy with either genomic, proteomic or metabolomic profiling form potential options. Better comparisons and study of underlying mechanisms in gut microbiome-based metabolic functions in obesity are urgently required. Today, an emerging field, focusing on metabolomic approaches and metabolic phenotyping, involved in high-throughput identification of metabolome in obesity and gut disorders, is involved in biomarker and metabolite identification. There are supporting technologies and approaches in NAFLD that throw light on the metabolites and gut microbiome, and also on the understanding of the risk factors of obesity along with liver cancer metabolic reaction networks. We discuss the current state of NAFLD metabolites, gut micro-environmental changes, and the further challenges in digital metabolomics profiling. Innovative clinical trial designs, with biomarker-enrichment strategies that are required to improve the outcome of NAFLD in patients are also discussed.

The pandemic of coronavirus disease 2019 (COVID-19) still remains on an upsurge trend. The second wave of this disease has led to panic in many countries, including India and some parts of the world suffering from the third wave. As there are no proper treatment options or remedies available for this deadly infection, supportive care equipment's such as oxygen cylinders, ventilators and heavy use of steroids play a vital role in the management of COVID-19. In the midst of this pandemic, the COVID-19 patients are acquiring secondary infections such as mucormycosis also known as black fungus disease. Mucormycosis is a serious, but rare opportunistic fungal infection that spreads rapidly, and hence prompt diagnosis and treatment are necessary to avoid high rate of mortality and morbidity rates. Mucormycosis is caused by the inhalation of its filamentous (hyphal form) fungi especially in the patients who are immunosuppressed. Recent studies have documented alarming number of COVID-19 patients with mucormycosis infection. Most of these patients had diabetes and were administered steroids for Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection and were consequently more prone to mucormycosis. Hence, the present review emphasizes mucormycosis and its related conditions, its mechanism in normal and COVID-19 affected individuals, influencing factors and challenges to overcome this black mold infection. Early identification and further investigation of this fungus will significantly reduce the severity of the disease and mortality rate in COVID-19 affected patients.

Platinum-based anticancer drugs (PADs), mainly cisplatin, carboplatin, and oxaliplatin, are widely used efficacious long-standing anticancer agents for treating several cancer types. However, clinicians worry about PAD chemotherapy and its induction of severe non-targeted organ toxicity. Compelling evidence has shown that toxicity of PAD on delicate body organs is associated with free radical generation, DNA impairment, endocrine and mitochondrial dysfunctions, oxidative inflammation, apoptosis, endoplasmic reticulum stress, and activation of regulator signaling proteins, cell cycle arrest, apoptosis, and pathways. The emerging trend is the repurposing of FDA-approved non-anticancer drugs (FNDs) for combating the side effects toxicity of PADs. Thus, this review chronicled the mechanistic preventive and therapeutic effects of FNDs against PAD organ toxicity in preclinical studies. FNDs are potential clinical drugs for the modulation of toxicity complications associated with PAD chemotherapy. Therefore, FNDs may be suggested as non-natural agent inhibitors of unpalatable side effects of PADs.

The human microbiome's role in colon and breast cancer is described in this review. Understanding how the human microbiome and metabolomics interact with breast and colon cancer is the chief area of this study. First, the role of the gut and distal microbiome in breast and colon cancer is investigated, and the direct relationship between microbial dysbiosis and breast and colon cancer is highlighted. This work also focuses on the many metabolomic techniques used to locate prospective biomarkers, make an accurate diagnosis, and research new therapeutic targets for cancer treatment. This review clarifies the influence of anti-tumor medications on the microbiota and the proactive measures that can be taken to treat cancer using a variety of therapies, including radiotherapy, chemotherapy, next-generation biotherapeutics, gene-based therapy, integrated omics technology, and machine learning.

Heavy metal Chromium (Cr), can adversely affect humans and their health if accumulated in organs of the body, such as the lungs, liver, and kidneys. Cr (VI) is highly toxic and has a higher solubility in water than Cr (III). One of the most common routes for Cr exposure is through inhalation and is associated with liver, lung, kidney damage, widespread dermatitis, GI tract damage, human lung cancer, cardiomyopathies, and cardiovascular disease. The increase in ROS production has been attributed to most of the damage caused by Cr toxicity. Cr-induced ROS-mediated oxidative stress has been seen to cause a redox imbalance affecting the antioxidant system balance in the body. The Nrf2 pathway dysregulation has been implicated in the same. Deregulation of histone acetylation and methylation has been observed, together with gene methylation in genes such as p16, MGMT, APC, hMLH1, and also miR-143 repression. Several ultra-structural changes have been observed following Cr (VI)-toxicity, including rough ER dilation, alteration in the mitochondrial membrane and nuclear membrane, pycnotic nuclei formation, and cytoplasm vacuolization. A significant change was observed in the metabolism of lipid, glucose, and the metabolism of protein after exposure to Cr. Cr-toxicity also leads to immune system dysregulations with changes seen in the expression of IL-8, IL-4, IgM, lymphocytes, and leukocytes among others. P53, as well as pro-and anti-apoptotic proteins, are involved in apoptosis. These Cr-induced damages can be alleviated via agents that restore antioxidant balance, regulate Nrf-2 levels, or increase anti-apoptotic proteins while decreasing pro-apoptotic proteins.

Doxorubicin is an extensively applied anti-cancerous drug since 1950′s and its usage is constrained because of its accumulation in a non-cancerous organ. Many studies have proven that doxorubicin causes reproductive toxicity depends on its dosage, particularly due to increased oxidative stress and apoptosis. A number of the researches have been carried out concerning its prevention. But there is a need to recognize the mechanism at the back of its toxicity to get better and improved method of treatment. To clarify the feasible mechanism of doxorubicin-mediated reproductive toxicity in rats, we have administrated doxorubicin at distinct dosages inclusive of low dosage (male rats that are at 230–250 g acquired cumulatively 1.5 mg/kg; ip; once per week for five weeks) and high dosage (male rats which are at 230–250 grams obtained cumulatively 15 mg/kg; ip; once every week for five weeks). Doxorubicin decreases antioxidant level such as GSH, Cu/Zn SOD, Mn SOD both in serum and testes. Increased oxidative stress is considered via elevated MDA level both in serum and testes. The level of ROS is measured via the DCFDA method in testes. Apoptosis become found through DNA fragmentation assay and quantification of Caspase 3, Caspase 9, Bcl2 and Cytochrome C. Doxorubicin mediated oxidative stress and apoptosis in testicular milieu is through deregulation of Nrf2, PGC-1α, AHR, ARNT, PXR, SUMO-1, UCP2, UCP3, ANX A5, Caspase 3, Caspase 9, Bcl2, Cytochrome C, GR, and GPX. In end, doxorubicin-mediated oxidative stress and apoptosis is through diverse transcriptional factors and genes with respect to decreased antioxidant level, augmented ROS level and Annexin A5 in the testicular milieu.

Arsenic is a ubiquitous metalloid compound commonly found in the environment, and it is usually found in combination with sulphur and metals. Arsenic is considered as a therapeutic as well as poisoning agent since ancient times. It causes toxic effects on different organs, mainly the liver. In this review, we focused on the molecular mechanism of arsenic-induced hepatotoxicity. Here we envisaged the bridge between arsenic and hepatotoxicity with particular focus on the level of hepatic enzymes such as ALT, AST, and ALP. Here, we attempted to elucidate the role of arsenic in redox imbalance on increased oxidative stress (elevated level of ROS, MDA and NO) and decreased antioxidant levels such as reduced GSH, catalase, and SOD. Oxidative stress induces mitochondrial dysfunction via apoptosis (AKT-PKB, MAPK, PI3/AKT, PKCδ-JNK, AKT/ERK, p53 pathways), fibrosis (TGF-β/Smad pathway), and necrosis and inflammation (TNF-α, NF-ĸB, IL-1, and IL-6). Along with that, arsenic activates caspases and Bax, decreases Bcl2 through mitochondrial dysfunction, and induces apoptosis regulatory mechanism. We believe the alteration of all these pathways leads to arsenic-induced hepatotoxicity.

Human coronaviruses, especially COVID-19, is an emerging pandemic infectious disease with high morbidity and mortality. Coronaviruses are associated with comorbidities, along with the symptoms of it. SARS-CoV-2 is one of the highly pathogenic coronaviruses that causes a high death rate compared to the SARS-CoV and MERS. In this review, we focused on the mechanism of coronavirus with comorbidities and impairment in multi-organ function. The main dysfunction upon coronavirus infection is damage to alveolar and acute respiratory failure. It is associated with the other organ damage such as cardiovascular risk via an increased level of hypertension through ACE2, gastrointestinal dysfunction, chronic kidney disease, diabetes mellitus, liver dysfunction, lung injury, CNS risk, ocular risks such as chemosis, conjunctivitis, and conjunctival hyperemia, cancer risk, venous thromboembolism, tuberculosis, aging, and cardiovascular dysfunction and reproductive risk. Along with this, we have discussed the immunopathology and coronaviruses at a molecular level and therapeutic approaches for the coronavirus infection. The comorbidities and multi-organ failure of COVID-19 have been explained at a molecular level along with the base of the SARS-CoV and MERS-CoV. This review would help us to understand the comorbidities associated with the coronaviruses with multi-organ damage., Graphical abstract Unlabelled Image

Adipose dysfunction is tightly associated with hepatic insulin resistance and steatosis condition. Doxorubicin would disturb the lipid metabolism both in adipose and liver. Here we projected that doxorubicin would impede lipogenesis and elevated lipolysis in adipose tissue would elevate the circulatory lipid profile and leads to insulin resistance. Further exacerbated lipid profile in circulation would impair the lipid metabolism in hepatic tissue which leads to fatty liver condition and consequently related disease during doxorubicin treatment. Doxorubicin impairs the lipogenesis through PPARγ and augments lipolysis and fatty acid oxidation through ATGL and PPARα in adipose tissue. Increased fatty acid level by adipose tissue in circulation would translocate into the liver and dysregulates AHR, PXR, PPARγ, ATGL and Apo B,which further develop insulin resistance and hepatic steatosis condition. The findings add to the mechanistic role of association between adipose tissue dysfunction and hepatic dysfunction.

The million-dollar question that has been the talk of the day is how effective the COVID 19 vaccines are against the Omicron variant. Still, there is no clear-cut answer to this question but several studies have concluded that this Variant of Concern (VOC) successfully weakens the neutralizing capability of the antibodies acquired from the COVID 19 vaccines and prior infections, which indicates that Omicron can easily bypass an individual's humoral immune response. However, the most significant confusion revolves around cell-mediated immunity tackling the Omicron variant. This paper aims to provide a clear idea about the status of the body's immune surveillance concerning the infection caused by the Omicron variant by producing the effectivity of the humoral and cell-mediated immunity in handling the same. This work also provides complete detail of the various characteristics of the Omicron variant and how it may be a blessing in disguise. The effectiveness of the current vaccines, the transmissibility rate of the variant compared to the other variants, and the importance of administering a booster dose to prevent the spread of this variant are also discussed. Finally, this work aims to bridge the gap between the past and the current status of the Omicron infection and sheds light on the hypothetical idea that herd immunity developed from the SARS-COV2 infection may help tackle other dangerous variants.