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Open AccessJournal ArticleDOI

Endothelium as a Source and Target of H2S to Improve Its Trophism and Function.

Valerio Ciccone, +2 more
- 19 Mar 2021 - 
- Vol. 10, Iss: 3, pp 486
TLDR
In this article, the beneficial autocrine/paracrine properties of hydrogen sulfide (H2S) on ECs and the state of the art on H2S potentiating drugs and tools are discussed.
Abstract
The vascular endothelium consists of a single layer of squamous endothelial cells (ECs) lining the inner surface of blood vessels. Nowadays, it is no longer considered as a simple barrier between the blood and vessel wall, but a central hub to control blood flow homeostasis and fulfill tissue metabolic demands by furnishing oxygen and nutrients. The endothelium regulates the proper functioning of vessels and microcirculation, in terms of tone control, blood fluidity, and fine tuning of inflammatory and redox reactions within the vessel wall and in surrounding tissues. This multiplicity of effects is due to the ability of ECs to produce, process, and release key modulators. Among these, gasotransmitters such as nitric oxide (NO) and hydrogen sulfide (H2S) are very active molecules constitutively produced by endotheliocytes for the maintenance and control of vascular physiological functions, while their impairment is responsible for endothelial dysfunction and cardiovascular disorders such as hypertension, atherosclerosis, and impaired wound healing and vascularization due to diabetes, infections, and ischemia. Upregulation of H2S producing enzymes and administration of H2S donors can be considered as innovative therapeutic approaches to improve EC biology and function, to revert endothelial dysfunction or to prevent cardiovascular disease progression. This review will focus on the beneficial autocrine/paracrine properties of H2S on ECs and the state of the art on H2S potentiating drugs and tools.

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Citations
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Endothelial Progenitor Cells Dysfunctions and Cardiometabolic Disorders: From Mechanisms to Therapeutic Approaches.

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The Role of Amino Acids in Endothelial Biology and Function

TL;DR: In this article , a review summarizes the metabolic and signaling pathways of AAs in ECs and discusses the importance of AA homeostasis in the functioning of ECs, and challenges in understanding the role of AA in the development of cardiovascular pathophysiology and possible directions for future research.
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Recent Advances in Molecular Research on Hydrogen Sulfide (H2S) Role in Diabetes Mellitus (DM)—A Systematic Review

TL;DR: This paper aims to synthesize and systematize, as comprehensively as possible, the recent literature-related data regarding the therapeutic/rehabilitative role of H2S in DM.
References
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Journal ArticleDOI

H2S as a Physiologic Vasorelaxant: Hypertension in Mice with Deletion of Cystathionine γ-Lyase

TL;DR: It is shown that H2S is physiologically generated by cystathionine γ-lyase (CSE) and that genetic deletion of this enzyme in mice markedly reduces H 2S levels in the serum, heart, aorta, and other tissues.
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The vasorelaxant effect of H2S as a novel endogenous gaseous KATP channel opener

TL;DR: It is demonstrated that H2S is an important endogenous vasoactive factor and the first identified gaseous opener of KATP channels in vascular SMCs and production from vascular tissues was enhanced by nitric oxide.
Journal ArticleDOI

Physiological Implications of Hydrogen Sulfide: A Whiff Exploration That Blossomed

TL;DR: The important life-supporting role of hydrogen sulfide (H(2)S) has evolved from bacteria to plants, invertebrates, vertebrate, vertebrates, and finally to mammals, but over the centuries it had only been known for its toxicity and environmental hazard.
Journal ArticleDOI

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TL;DR: In this review the main endothelial abnormalities found in various human diseases such as cancer, diabetes mellitus, atherosclerosis, and viral infections are addressed.
Journal ArticleDOI

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TL;DR: It is concluded that NO is a downstream imperative of VEGF-, but not bFGF-induced angiogenesis, and it is proposed that the NO synthase/guanylate cyclase pathway is a potential target for controlling tumorAngiogenesis in response to V EGF.
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