Tree of life: endothelial cell in norm and disease, the good guy is a partner in crime!

Abstract

Undeniably, endothelial cells (EC) contribute to the maintenance of the homeostasis of the organism through modulating cellular physiology, including signaling pathways, through the release of highly active molecules as well as the response to a myriad of extrinsic and intrinsic signaling factors. Review the data from the current literature on the EC role in norm and disease. Endothelium maintains a precise balance between the released molecules, where EC dysfunction arises when the endothelium actions shift toward vasoconstriction, the proinflammatory, prothrombic properties after the alteration of nitric oxide (NO) production and oxidative stress. The functions of the EC are regulated by the negative/ positive feedback from the organism, through EC surface receptors, and the crosstalk between NO, adrenergic receptors, and oxidative stress. More than a hundred substances can interact with EC. The EC dysfunction is a hallmark in the emergence and progression of vascular-related pathologies. The paper concisely reviews recent advances in EC (patho) physiology. Grasping EC physiology is crucial to gauge their potential clinical utility and optimize the current therapies as well as to establish novel nanotherapeutic molecular targets include; endothelial receptors, cell adhesion molecules, integrins, signaling pathways, enzymes; peptidases.

Single Cross-Sectional Analysis; Post-Myocardial Infarction Instrumental & Laboratory changes in Prognosis Behavior

“…The high level of leukocytes in diabetic patients endorses the hypothesis of a mild chronic mild inflammatory syndrome in patients with metabolic syndrome [9, 21, 23, 28]. The high TAG values in diabetic patients are due to lipogenesis from high glucose serum levels and metabolic disorders associated with chronic lipid peroxidation and biogenesis disorders [28, 29].…”

“…Lifestyle changes have a huge impact on the overall health of the cardiovascular system [3,4]. Unfortunately, sedentary lifestyle is seen in majority of myocardial infarction, which is associated with development of several predisposition factors for cardiovascular events such as dyslipidaemia, insulin resistance, and central obesity or visceral obesity [5][6][7][8][9]. Collectively, these early signs of disturbance of cardiovascular homeostasis are ignored to provoke the progression of dyslipidaemia and insulin resistance to reach enough levels to induce the emergence of cardiovascular events such as MI [10,11].…”

“…The role of these changes is unclear in determining the prognosis of patients with MI and the potential risk of developing complications such as renal failure. In the current retrospective analysis, we covered the potential role of these systemic and the regularly checked cardiac markers in the prognosis determination and prognosis of the patients [5, 8, 20–23, 9, 13–19].…”

Early Prognostic Instrumental and Laboratory Biomarkers in Post-MI

“…Many aspects of post-myocardial infarction (MI) changes remain unclear and require further investigation. Consequently, determining the precise life expectancy of MI patients remains challenging [6][7][8]. MI involves necrosis of myocardiocytes and disruption of the heart tissue's essential functions, including automaticity, conduction, and contractility.…”

“…The pathophysiology of MI involves an imbalance between myocardial oxygen demand and supply [11,12]. Subsequently, cardiac cells experience ischemia, leading to sequelae such as oxidative stress due to mitochondrial and cellular membrane deterioration [7,[13][14][15][16][17][18][19][20][21][22][23]. The lipid content of membranes plays a crucial role in cardiac cells regarding ischemia tolerance.…”