Background and Aims: Metabolic syndrome is a multifactorial pathophysiological process with complicated homeostatic disorders that arise from various systematic metabolic defects. Various theories underlie the development of metabolic syndrome but are fully not understood. Methods: Revising PubMed and Scopus literature data on metabolic syndrome pathogenesis and management. Results: The most accepted hypothesis is that a cluster of risk factors combined to obtain a truly metabolic syndrome. The pathophysiology of the metabolic syndrome depends on the underlying development path due to insulin resistance or chronic inflammation and is usually combined with neurohormonal disturbance. Meanwhile, these defects can be inherited via loss of function of certain genes that lead to severe obesity, early diabetes, or severe insulin resistance (with or without lipodystrophy). Chronic inflammation is also a driver of metabolic syndrome. Lifestyle is still the therapy of choice in managing metabolic syndrome, but unfortunately, during the lockdown, most people could not reserve a healthy regime; therefore, it can also be referred to as a pandemic with COVID-19. Conclusions: This powerful illustration shows how defects in specific encoded proteins located predominantly in the brain, pancreatic beta-cell, muscle, or fat give rise to these distinct components of the metabolic syndrome. Primarily, obesity and its sequela are the initiators of metabolic syndrome. The presence of metabolic syndrome increases the risk and severity of other pathologies' emergence, even in non-related metabolic syndrome diseases such as COVID-19. The article provides new insights into the pathogeneses and management of the metabolic syndrome.

Introduction. Lipid is an essential component of the cell and its organelles membrane. The uniqueness and selectivity of lipids to specific functions and asymmetry of lipid distribution in the organelle’s membrane give the cell ability of being highly qualified and specified. Aim. The paper provides a comprehensive review of membrane lipids in different tissues and organelles of the cell in norm and disease. Material and methods. The paper analyzed the present literature data on membrane lipids behavior in physiology and pathology. Analysis of the literature. The major structural and functional lipids of the cell membrane are phosphatidylcholine > phosphatidylethanolamine. The absence/deficiency or augmentation of a specific type of lipid results in serious defects and usually life-threatening with a permanent disability. The observations discussed here suggest, the lipid peroxidation severity depends on the membrane lipid composition of the cell. Some tissue cells can handle lipoperoxidation and protect themselves from the peroxidation damaging products better, while other cells cannot compensate. Therefore, some organs are highly sensitive to peroxidation and irreversible changes occur rapidly. Conclusion. To sum up, the understanding of lipid’s role in norm and disease is clinically crucial to evaluate a novel therapeutic target to treat many metabolic disorders such as metabolic syndrome and some lysosomal storage disorders via targeting specific new signaling pathways, lipid molecules, and enzymes.

Myocardial infarction and its sequalae remain the leading cause of death worldwide. Myocardial infarction (MI) survivors continue to live a poor quality of life due to extinguished heart failure. The post-MI period involves several changes at the cellular and subcellular levels, of which autophagy dysfunction. Autophagy is involved in the regulation of post-MI changes. Physiologically, autophagy preserves intracellular homeostasis by regulating energy expenditure and sources. Furthermore, dysregulated autophagy is considered the hallmark of the post-MI pathophysiological changes, which leads to the known short and long post-MI reperfusion injury sequalae. Autophagy induction strengthens self-defense mechanisms of protection against energy deprivation through economic energy sources and uses alternative sources of energy through the degradation of intracellular components of the cardiomyocyte. The protective mechanism against post-MI injury includes the enhancement of autophagy combined with hypothermia, which induces autophagy. However, several factors regulate autophagy, including starvation, nicotinamide adenine dinucleotide (NAD+), Sirtuins, other natural foods and pharmacological agents. Autophagy dysregulation involves genetics, epigenetics, transcription factors, small noncoding RNAs, small molecules, and special microenvironment. Autophagy therapeutic effects are signaling pathway-dependent and MI stage dependent. The paper covers recent advances in the molecular physiopathology of autophagy in post-MI injury and its potential target as a future therapeutic strategy.

Undeniably, lipid plays an extremely important role in the homeostasis balance since lipid contributes to the regulation of the metabolic processes. The metabolic syndrome pathogenesis is multi-pathway that composes neurohormonal disorders, endothelial cell dysfunction, metabolic disturbance, genetic predisposition, in addition to gut commensal microbiota. The heterogenicity of the possible mechanisms gives the metabolic syndrome its complexity and limitation of therapeutic accesses. The main pathological link is that lipid contributes to the emergence of metabolic syndrome via central obesity and visceral obesity that consequently lead to oxidative stress and chronic inflammatory response promotion. Physiologically, a balance is kept between the adiponectin and adipokines levels to maintain the lipid level in the organism. Clinically, extremely important to define the borders of the lipid level in which the pathogenesis of the metabolic syndrome is reversible, otherwise it will be accompanied by irreversible complications and sequelae of the metabolic syndrome (cardiovascular, insulin resistance). The present paper is dedicated to providing novel insights into the role of lipid in the development of metabolic syndrome; hence dyslipidemia is the initiator of insulin resistance syndrome (metabolic syndrome).

Background: The regeneration strategy involves several aspects, such as reprogramming aspects, targeting pathophysiological processes, and inducing the physiological one. Autophagy targeting is a potential physiological/pathogenetic strategy to enhance myocardiocytes' function. Myocardiocytes' injury-related death remains to be the highest in our era. Unfortunately, myocardiocytes have a limited proliferation capacity to compensate for what was lost by infarction. However, partially injured myocardiocytes can be preserved by improving the autophagy process of myocardiocytes. Main text: Autophagy induction involved controlling the cellular and subcellular environment as well as gene expression. Autophagy is well known to prolong the longevity of cell and human life. Inhibition of the mTOR receptor, proapoptotic gene Bnip3, IP3, and lysosome inhibitors, inhibition of microRNA-22 and overexpression of microRNA-99a, modulators of activated protein kinase with adenosine monophosphate, resveratrol, sirtuin activators, Longevinex and calcium lowering agents can promote physiological myocardiocyte autophagy and improve post-myocardial modulation and recovery speed. The paper aimed to assess autophagy role in myocardiocytes regeneration modulation. Conclusions: The autophagy strategy can be applied to infarcted myocardiocytes, as well as heart failure. However, cell self-eating is not the preferred therapy for preserving injured myocardiocytes or causing regeneration.