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Serum/glucocorticoid-regulated kinase 1 (SGK1), a member of the serine/threonine protein kinase gene family, is primarily regulated by serum and glucocorticoids. SGK1 is involved in the development of tumors and fibrotic diseases. However, relatively little research has been conducted on their role in immune and inflammatory diseases. SGK1 may act as a pivotal immune regulatory gene by modulating immune cells (e.g., T cells, macrophages, dendritic cells, and neutrophils) and functions and is involved in the pathogenesis of some immune and inflammatory diseases, such as inflammatory bowel disease, multiple sclerosis, allergic diseases, sepsis, and major depressive disorder. This review aims to provide an overview of the latest research focusing on the immune and inflammatory regulatory roles of SGK1 and provide new insights into diagnostic and therapeutic approaches for immune and inflammatory diseases. [ABSTRACT FROM AUTHOR]

Lactate dehydrogenase (LDH) is a terminating enzyme in the metabolic pathway of anaerobic glycolysis with end product of lactate from glucose. The lactate formation is crucial in the metabolism of glucose when oxygen is in inadequate supply. Lactate can also be formed and utilised by different cell types under fully aerobic conditions. Blood LDH is the marker enzyme, which predicts mortality in many conditions such as ARDS, serious COVID-19 and cancer patients. Lactate plays a critical role in normal physiology of humans including an energy source, a signaling molecule and a pH regulator. Depending on the pH, lactate exists as the protonated acidic form (lactic acid) at low pH or as sodium salt (sodium lactate) at basic pH. Lactate can affect the immune system and act as a signaling molecule, which can provide a "danger" signal for life. Several reports provide evidence that the serum lactate represents a chemical marker of severity of disease similar to LDH under inflammatory conditions. Since the mortality rate is much higher among COVID-19 patients, associated with high serum LDH, this article is aimed to review the LDH as a therapeutic target and lactate as potential marker for monitoring treatment response of inflammatory diseases. Finally, the review summarises various LDH inhibitors, which offer potential applications as therapeutic agents for inflammatory diseases, associated with high blood LDH. Both blood LDH and blood lactate are suggested as risk factors for the mortality of patients in serious inflammatory diseases. [ABSTRACT FROM AUTHOR]

Inflammation is a universal response mechanism existing as inter-communicator of biological systems. Uncontrolled or dysregulated inflammation addresses chronic low-grade effects eventually resulting in multimorbidity. Active solute transport across the membrane establishes varying osmotic gradients. Aquaporins (AQPs) are a class of critical ubiquitously expressed transmembrane proteins that aid in fluid and small solute transport via facilitated diffusion over established osmotic gradients. Numerous significant data features the biological functions of AQPs rendering them as an appropriate biomarker of health and diseases. Besides their physiological role in well-balanced inflammatory responses, it is worth noting the dysregulation of AQPs during any undesirable inflammatory event. Most literature to date clearly sets out AQPs as potential drug targets instigating AQP-based therapies. In light of this conception, the current review provides a compendious overview on the propitious and portentous out-turns of AQPs under inflammation. [ABSTRACT FROM AUTHOR]

Mitophagy is a metabolic process to remove excessive or damaged mitochondria in eukaryotic cells. It is well-known that mitochondria are one of the major sources of reactive oxygen species (ROS). Mitochondrial ROS and damage-associated molecular patterns (DAMPs) can activate inflammasomes to induce inflammatory responses. Once the activation is regulated improperly, excessive inflammation will bring about various tissue injuries, resulting in a series of diseases. However, the selective mitochondrial autophagy can specifically eliminate dysfunctional mitochondria to maintain mitochondrial homeostasis and protect against the hyperinflammation induced by ROS and DAMPs. Recent studies demonstrated that a variety of internal and external factors regulate several inflammatory diseases via altering the level of mitophagy. In this review, we summarize the latest research progress of mitophagy and focus on the inflammatory responses regulated by mitophagy, aiming to illuminate the role of mitophagy in inflammation and provide clues to the diagnosis and therapy of inflammatory diseases. [ABSTRACT FROM AUTHOR]

Physalis minima has been traditionally used as a folk herbal medicine in China for the treatment of many inflammatory diseases. However, little is known about its anti-inflammatory constituents and associated molecular mechanisms. In our study, withaphysalin A (WA) and 2, 3-dihydro-withaphysalin C (WC), two major withanolide-type compounds, were obtained from the anti-inflammatory fraction of P. minima. Both WA and WC significantly inhibited the production of nitrite oxide (NO), prostaglandin E (PGE), and several pro-inflammatory cytokines, such as interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) in lipopolysaccharide (LPS)-activated RAW264.7 macrophages. Further research indicated that they downregulated the LPS-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the mRNA and protein levels. In addition, they also suppressed nuclear translocation of NF- κB p65, phosphorylation of STAT3, and upregulated HO-1 expression. Intriguingly, the activation of MAPKs was suppressed by WA but was not altered by WC. Taken together, these data provide scientific evidence for elucidating the major bioactive constituents and related molecular mechanisms for the traditional use of P. minima and suggest that WA and WC can be attractive therapeutic candidates for various inflammatory diseases. [ABSTRACT FROM AUTHOR]