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. 2022 Dec:30:100614.
doi: 10.1016/j.cophys.2022.100614. Epub 2022 Nov 4.

Recent Insights Concerning Autophagy and Endothelial Cell Nitric Oxide Generation

Seul-Ki Park  1 , Jae Min Cho  2   3 , Sohom Mookherjee  1 , Paulo W Pires  4 , J David Symons  1   5
Affiliations

Recent Insights Concerning Autophagy and Endothelial Cell Nitric Oxide Generation

Seul-Ki Park et al. Curr Opin Physiol. 2022 Dec.

Abstract

Although endothelial cell (EC) dysfunction contributes to the etiology of more diseases than any other tissue in the body, EC metabolism is an understudied therapeutic target. Evidence regarding the important role of autophagy in maintaining EC homeostasis is accumulating rapidly. Here we focus on advances over the past two years regarding how EC autophagy mediates EC nitric oxide generation in the context of aging and cardiovascular complications including coronary artery disease, aneurysm, and stroke. In addition, insight concerning the efficacy of maneuvers designed to boost EC autophagy in an effort to combat cardiovascular complications associated with repressed EC autophagy is discussed.

Keywords: Aging; aneurysm; atherosclerosis; coronary artery disease; stroke.

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Conflict of interest statement

Conflict of interest statement All authors have nothing to declare.

Figures

Figure 1.
Figure 1.. Recent research.
The number of publications identified by keywords “autophagy and endothelial cell” has grown over the past decade (A). This review focused upon publications selected from 41 that were identified by keywords “autophagy and endothelial cell and nitric oxide” from 2020, 2021, and between January and July 2022 (B).
Figure 2.
Figure 2.. EC autophagy impacts EC NO generation.
Evidence exists that EC autophagy is repressed in the context of aging and cardiovascular complications including coronary artery disease, aneurysm, and stroke. Amplifying whole body or arterial EC autophagy might improve outcomes in each context by improving nitric oxide (NO) bioavailability. The numbers in brackets refer to the specific citation. EDHF, endothelium-derived hyperpolarizing factor; EDCF, endothelium-derived constricting factor; TSA, trichostatin A; NMN: nicotinamide mononucleotide.
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