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Cardiovascular disease (CAD) is the main cause of morbidity and deaths in the western world. The development of atherosclerosis underlying CAD development begins early in human life. There are numerous genetic and environmental risk factors accelerating its progression which then leads to the occurrence of acute events. Despite considerable progress in determining risk factors, there is still a lot of work ahead since identified determinants are responsible only for a part of overall CAD risk. Current therapies are insufficient to successfully reduce the risk of atherosclerosis development. Therefore, there is a need for effective preventive measures of clinical manifestations of atherosclerosis since the currently available drugs cannot prevent the occurrence of even 70% of clinical events. The shift of the target from lipid metabolism has opened the door to many new therapeutic targets. Currently, the majority of known targets for anti-atherosclerotic drugs focus also on inflammation (a common mediator of many risk factors), mechanisms of innate and adaptive immunity in atherosclerosis, molecule scavengers, etc. The therapeutic potential of cyclodextrins, protein kinase inhibitors, colchicine, inhibitors of p38 mitogen-activated protein kinase (MAPK), lipid dicarbonyl scavengers, a monoclonal antibody targeting interleukin-1β, and P-selectin inhibitors is still not fully confirmed and requires confirmation in large clinical trials. The preliminary results look promising.

Anemia is frequently observed in the course of chronic kidney disease (CKD) and it is associated with diminishing the quality of a patient's life. It also enhances morbidity and mortality and hastens the CKD progression rate. Patients with CKD frequently suffer from a chronic inflammatory state which is related to a vast range of underlying factors. The results of studies have demonstrated that persistent inflammation may contribute to the variability in Hb levels and hyporesponsiveness to erythropoietin stimulating agents (ESA), which are frequently observed in CKD patients. The understanding of the impact of inflammatory cytokines on erythropoietin production and hepcidin synthesis will enable one to unravel the net of interactions of multiple factors involved in the pathogenesis of the anemia of chronic disease. It seems that anti-cytokine and anti-oxidative treatment strategies may be the future of pharmacological interventions aiming at the treatment of inflammation-associated hyporesponsiveness to ESA. The discovery of new therapeutic approaches towards the treatment of anemia in CKD patients has become highly awaited. The treatment of anemia with erythropoietin (EPO) was associated with great benefits for some patients but not all.

Depressive disorders are heterogeneous in nature, and their global reach makes them the cause of suffering for a million individuals worldwide. Standard treatment does not work for one in three people, and side effects can significantly reduce the quality of life. A multidisciplinary approach allows for a broader insight into the nature of the disease, given its complex etiology. One of its elements is the hypothesis of inflammation, which also accompanies obesity-related disease. Obesity and depression interact, causing many researchers to develop new non-pharmacological treatment methods for both diseases. One suggestion is physical exercises that have great potential to be used in clinical practice. They can exert changes on the central nervous system and thus modulate mood. Another is diet, which concentrates on active molecules that also affect the central nervous system (CNS). There is an urgent need to create appropriate criteria and recommendations that systematize existing knowledge and allow it to be used in practice. There is an urgent need to create appropriate criteria and recommendations that systematize existing knowledge and allow it to be used in practice. [ABSTRACT FROM AUTHOR]

Atherosclerosis is one of the most fatal diseases in the world. The associated thickening of the arterial wall and its background and consequences make it a very composite disease entity with many mechanisms that lead to its creation. It is an active process, and scientists from various branches are engaged in research, including molecular biologists, cardiologists, and immunologists. This review summarizes the available information on the pathophysiological implications of atherosclerosis, focusing on endothelium dysfunction, inflammatory factors, aging, and uric acid, vitamin D, and miRNA expression as recent evidence of interactions of the molecular and cellular elements. Analyzing new discoveries for the underlying causes of this condition assists the general research to improve understanding of the mechanism of pathophysiology and thus prevention of cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Chronic kidney disease (CKD) is a serious health problem that can affect various systems in the human body. Renal failure promotes mechanisms of premature cellular aging and also features of generalized inflammation in the body, which translates into a close relationship between kidney dysfunction and cardiovascular disease (CVD). As kidney function deteriorates, cardiovascular risk and mortality increase in this group of patients. Oxidative stress and inflammation are two closely related processes that initiate a vicious cycle by activating each other. Together with aging, they represent the key factors that cause and exacerbate CVD in CKD. Patients with CKD are particularly vulnerable to the accumulation of aging endothelial cells, vascular smooth muscle and macrophages, increasing the risk of atherosclerosis. Several mechanisms are known that can lead to the progression of the aforementioned problems, such as the accumulation of uremic toxins, persistent inflammation, impaired lipid and electrolyte metabolism, nitric oxide (NO) deficiency, the increased production of reactive oxygen species (ROS) and damage to deoxyribonucleic acid (DNA) and mitochondria. According to research, we can distinguish a group of drugs that effectively counteract the negative effects of CKD—statins. This is a group of drugs that inhibit 3-hydroxy-3-methylglutaryl-coenzyme-A (HMG-CoA) reductase and affect a number of cellular processes and pathways, resulting in the overall slowing of atherosclerosis and cellular aging. [ABSTRACT FROM AUTHOR]

Rheumatic heart disease (RHD), an acquired valvular disease, remains an important cause of morbidity and mortality in developing countries. This chronic illness starts from untreated streptococcal throat infection, resulting in acute rheumatic fever (ARF) in susceptible individuals. Repeated infections lead to a chronic phase characterized by the damage of heart valves. Inflammation has been found to play important role in the development of this disease. All the studies presented in this review clearly show the involvement of the inflammatory state in the progression of this disease. However, the exact role of cytokines in inflammation sites remains to be examined, since most studies have so far focused on peripheral blood. Such analysis would provide information on inflammatory mechanisms in situ. [ABSTRACT FROM AUTHOR]

Diabetes is considered a new pandemic of the modern world, and the number of sufferers is steadily increasing. Sustained hyperglycemia promotes the production of free radicals and leads to persistent, low-grade inflammation. Oxidative stress causes mitochondrial destruction, which along with activation of the hexosamine pathway, nuclear factor-κB (Nf-κb), p38 mitogen-activated protein kinase (p38 MAPK), c-jun NH2 terminal kinase/stress-activated protein kinase (JNK/SAPK) or toll-like receptors (TLRs), leads to pancreatic β-cell dysfunction. However, there is also the protective mechanism that counteracts oxidative stress and inflammation in diabetes, mitophagy, which is a mitochondrial autophagy. An important part of the strategy to control diabetes is to lead a healthy lifestyle based on, among other things, regular physical activity, giving up smoking, eating a balanced diet containing ingredients with antioxidant potential, including vegetables and fruits, and using hypoglycemic pharmacotherapy. Tobacco smoke is a recognized modifiable risk factor for many diseases including diabetes, and it has been shown that the risk of the disease increases in proportion to the intensity of smoking. Physical activity as another component of therapy can effectively reduce glucose fluctuations, and high intensity interval exercise appears to have the most beneficial effect. A proper diet not only increases cellular sensitivity to insulin, but is also able to reduce inflammation and oxidative stress. Pharmacotherapy for diabetes can also affect oxidative stress and inflammation. Some oral drugs, such as metformin, pioglitazone, vildagliptin, liraglutide, and exenatide, cause a reduction in markers of oxidative stress and/or inflammation, while the new drug Imeglimin reverses pancreatic β-cell dysfunction. In studies of sitagliptin, vildagliptin and exenatide, beneficial effects on oxidative stress and inflammation were achieved by, among other things, reducing glycemic excursions. For insulin therapy, no corresponding correlation was observed. Insulin did not reduce oxidative stress parameters. There was no correlation between glucose variability and oxidative stress in patients on insulin therapy. The data used in this study were obtained by searching PubMed online databases, taking into account recent studies. [ABSTRACT FROM AUTHOR]

Chronic kidney disease (CKD) is a major public health problem with a developing incidence and prevalence. As a consequence of the growing number of patients diagnosed with renal dysfunction leading to the development of CKD, it is particularly important to explain the mechanisms of its underlying causes. In our paper, we discuss the molecular mechanisms of the development and progression of CKD, focusing on oxidative stress, the role of the immune system, neutrophil gelatinase-associated lipocalin, and matrix metalloproteinases. Moreover, growing evidence shows the importance of the role of the gut–kidney axis in the maintenance of normal homeostasis and of the dysregulation of this axis in CKD. Further, we discuss the therapeutic potential and highlight the future research directions for the therapeutic targeting of CKD. However, additional investigation is crucial to improve our knowledge of CKD progression and, more importantly, accelerate basic research to improve our understanding of the mechanism of pathophysiology. [ABSTRACT FROM AUTHOR]

Coronary artery spasm (CAS) is a reversible phenomenon caused by spontaneous excessive vascular smooth muscle contractility and vascular wall hypertonicity, which results in partial or complete closure of the lumen of normal or atherosclerotic coronary arteries. The clinical picture of CAS includes chest discomfort which is similar in quality to that of stable effort angina. Mechanisms underlying the development of CAS are still unclear. CAS certainly is a multifactorial disease. In this review, we paid attention to the role of the main pathophysiologic mechanisms in CAS: endothelial dysfunction, chronic inflammation, oxidative stress, smooth muscle hypercontractility, atherosclerosis and thrombosis, and mutations leading to deficient aldehyde dehydrogenase 2 (ALDH2) activity. These findings might shed novel insight on the underlying mechanisms and identify potential diagnostic and therapeutic targets for cardiovascular diseases in the future. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases (CVDs) are disorders associated with the heart and circulatory system. Atherosclerosis is its major underlying cause. CVDs are chronic and can remain hidden for a long time. Moreover, CVDs are the leading cause of global morbidity and mortality, thus creating a major public health concern. This review summarizes the available information on the pathophysiological implications of CVDs, focusing on coronary artery disease along with atherosclerosis as its major cause and arterial hypertension. We discuss the endothelium dysfunction, inflammatory factors, and oxidation associated with atherosclerosis. Mechanisms such as dysfunction of the endothelium and inflammation, which have been identified as critical pathways for development of coronary artery disease, have become easier to diagnose in recent years. Relatively recently, evidence has been found indicating that interactions of the molecular and cellular elements such as matrix metalloproteinases, elements of the immune system, and oxidative stress are involved in the pathophysiology of arterial hypertension. Many studies have revealed several important inflammatory and genetic risk factors associated with CVDs. However, further investigation is crucial to improve our knowledge of CVDs progression and, more importantly, accelerate basic research to improve our understanding of the mechanism of pathophysiology. [ABSTRACT FROM AUTHOR]

Cancers are a frequent cause of morbidity and mortality. There are many risk factors for tumours, including advanced age, personal or family history of cancer, some types of viral infections, exposure to radiation and some chemicals, smoking and alcohol consumption, as well as obesity. Increasing evidence suggest the role of obesity in the initiation and progression of various cancers, including renal cell carcinoma. Since tumours require energy for their uncontrollable growth, it appears plausible that their initiation and development is associated with the dysregulation of cells metabolism. Thus, any state characterised by an intake of excessive energy and nutrients may favour the development of various cancers. There are many factors that promote the development of renal cell carcinoma, including hypoxia, inflammation, insulin resistance, excessive adipose tissue and adipokines and others. There are also many obesity-related alterations in genes expression, including DNA methylation, single nucleotide polymorphisms, histone modification and miRNAs that can promote renal carcinogenesis. This review focuses on the impact of obesity on the risk of renal cancers development, their aggressiveness and patients' survival. [ABSTRACT FROM AUTHOR]

Arterial hypertension (AH) is a major cause of cardiovascular diseases (CVD), leading to dysfunction of many organs, including the heart, blood vessels and kidneys. AH is a multifactorial disease. It has been suggested that the development of each factor is influenced by oxidative stress, which is characterized by a disturbed oxidant-antioxidant balance. Excessive production of reactive oxygen species (ROS) and an impaired antioxidant system promote the development of endothelial dysfunction (ED), inflammation and increased vascular contractility, resulting in remodeling of cardiovascular (CV) tissue. The hope for restoring the proper functioning of the vessels is placed on antioxidants, and pharmacological strategies are still being sought to reverse the harmful effects of free radicals. In our review, we focused on the correlation of AH with oxidative stress and inflammation, which are influenced by many factors, such as diet, supplementation and pharmacotherapy. Studies show that the addition of a single dietary component may have a beneficial effect on blood pressure (BP) values; however, the relationship between the antioxidant/anti-inflammatory properties of individual dietary components and the hypotensive effect is not clear. Moreover, AH pharmacotherapy alleviates the increased oxidative stress, which may help prevent organ damage. [ABSTRACT FROM AUTHOR]