Endothelial dysfunction and its relation in different disorders: Recent update

Ray, Adarsh; Maharana, Krushna Ch.; Meenakshi, Sarasa; Singh, Sanjiv

doi:10.1016/j.hsr.2023.100084

Cited by 27 publications

(14 citation statements)

References 114 publications

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“…The primary mechanism underlying endothelial dysfunction (ED) involves a reduction in the formation and bioavailability of nitric oxide (NO), accompanied by a concurrent increase in the level of superoxide ions and the production of active vasoconstrictors [245,246]. Consequently, ED manifests as an imbalance between mediators crucial for the optimal functioning of all endotheliumdependent processes under normal conditions [247].…”

Section: No and Endothelial Dysfunctionmentioning

confidence: 99%

Nitric Oxide in the Mechanisms of Cell Death and Cytoprotection

Belenichev,

Popazova,

Bukhtiyarova

et al. 2024

Preprint

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The regulation of cell death is a fundamental issue in cell biology and continues to be intensely investigated worldwide. The significance of research in this field persists because understanding the determinants of cell lifespan directly impacts the maintenance of multicellular organism homeostasis and, consequently, is crucial for addressing biomedical challenges associated with various diseases. It is recognized that the initiation of cell death can be prompted by both specific signals (such as cytokines or hormones) and nonspecific stimuli, including radiation, temperature increase, or oxidants. When these factors affect a cell, numerous signaling pathways are triggered in the cell, leading to neutralization of the effects of their negative effects or, in case of irreparable damage, to cell elimination. This removal of damaged cells occurs through apoptosis or programmed cell death, a highly regulated process. Numerous signaling molecules participate in orchestrating the apoptotic process, many of which also govern other essential functions within the organism. Physiological factors capable of triggering the apoptotic program in cells include nitric oxide (NO), which serves as one of the key signaling molecules regulating the functions of the cardiovascular, nervous, and immune systems of the organism. The unique chemical nature of NO, along with its numerous intracellular targets and physiologically active redox forms, raises questions about the specific mechanisms through which NO exerts its damaging effects on cells. Utilizing pharmacological preparations- such as sources (donors) of exogenous nitric oxide- represents an approach to investigating the initiation and execution of the apoptotic program in sensitive target cells. Furthermore, this approach holds promise as a direction for discovering new selective drugs.

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Section: No and Endothelial Dysfunctionmentioning

confidence: 99%

Nitric Oxide in the Mechanisms of Cell Death and Cytoprotection

Belenichev,

Popazova,

Bukhtiyarova

et al. 2024

Preprint

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“…1 When vascular endothelial dysfunction and damage occur, they give rise to pathological conditions such as abnormal vascular tone, inflammatory responses, and thrombosis, all of which are risk factors associated with the development of CVDs. 2,3 Endothelial-to-mesenchymal transition (EndMT) is a complex physiological process involving the cellular transition from ECs to a mesenchymal phenotype, which may play an important role in embryonic development and disease progression. 4 This process results in the loss of cellular adhesion, changes in cytoskeletal organization, and the promotion of the migratory and invasive abilities of ECs.…”

Section: Introductionmentioning

confidence: 99%

“…ECs play a prominent role in the pathogenesis of various CVDs by releasing vasoactive substances 1 . When vascular endothelial dysfunction and damage occur, they give rise to pathological conditions such as abnormal vascular tone, inflammatory responses, and thrombosis, all of which are risk factors associated with the development of CVDs 2,3 …”

Section: Introductionmentioning

confidence: 99%

Melatonin alleviates myocardial dysfunction through inhibition of endothelial‐to‐mesenchymal transition via the NF‐κB pathway

Kim,

Jeong

et al. 2024

Journal of Pineal Research

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Endothelial‐to‐mesenchymal transition (EndMT) is a complex biological process of cellular transdifferentiation by which endothelial cells (ECs) lose their characteristics and acquire mesenchymal properties, leading to cardiovascular remodeling and complications in the adult cardiovascular diseases environment. Melatonin is involved in numerous physiological and pathological processes, including aging, and has anti‐inflammatory and antioxidant activities. This molecule is an effective therapeutic candidate for preventing oxidative stress, regulating endothelial function, and maintaining the EndMT balance to provide cardiovascular protection. Although recent studies have documented improved cardiac function by melatonin, the mechanism of action of melatonin on EndMT remains unclear. The present study investigated the effects of melatonin on induced EndMT by transforming growth factor‐β2/interleukin‐1β in both in vivo and in vitro models. The results revealed that melatonin reduced the migratory ability and reactive oxygen species levels of the cells and ameliorated mitochondrial dysfunction in vitro. Our findings indicate that melatonin prevents endothelial dysfunction and inhibits EndMT by activating related pathways, including nuclear factor kappa B and Smad. We also demonstrated that this molecule plays a crucial role in restoring cardiac function by regulating the EndMT process in the ischemic myocardial condition, both in vessel organoids and myocardial infarction (MI) animal models. In conclusion, melatonin is a promising agent that attenuates EC dysfunction and ameliorates cardiac damage compromising the EndMT process after MI.

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“…However, under certain conditions, such as an excess of nutrients or the induction of alternative biochemical pathways, more molecules are generated and the protection mechanisms at the cellular level are overwhelmed, which creates a toxic environment for cells and consequently for the organism [ 17 , 18 ]. In this context, incorporating compounds, additives or molecules to reduce the concentration of free radicals and generate a better cellular response [ 19 , 20 ] would promote the health and growth of production animals [21] .…”

Section: Introductionmentioning

confidence: 99%

Exploring the metabolic and antioxidant potential of solergy: Implications for enhanced animal production

Olivares-Ferretti,

Chavez,

Maguregui

et al. 2024

Biotechnology Reports

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Endothelial dysfunction and its relation in different disorders: Recent update

Cited by 27 publications

References 114 publications

Nitric Oxide in the Mechanisms of Cell Death and Cytoprotection

Nitric Oxide in the Mechanisms of Cell Death and Cytoprotection

Melatonin alleviates myocardial dysfunction through inhibition of endothelial‐to‐mesenchymal transition via the NF‐κB pathway

Exploring the metabolic and antioxidant potential of solergy: Implications for enhanced animal production

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