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Review
. 2023 Jun 27:14:1191426.
doi: 10.3389/fendo.2023.1191426. eCollection 2023.

Physiological and pathological characteristics of vascular endothelial injury in diabetes and the regulatory mechanism of autophagy

Hanyu Liu  1 , Xueru Wang  1 , Hong Gao  1   2 , Chan Yang  3 , Chunguang Xie  1   2
Affiliations
Review

Physiological and pathological characteristics of vascular endothelial injury in diabetes and the regulatory mechanism of autophagy

Hanyu Liu et al. Front Endocrinol (Lausanne). .

Abstract

Vascular endothelial injury in diabetes mellitus (DM) is the major cause of vascular disease, which is closely related to the occurrence and development of a series of vascular complications and has a serious negative impact on a patient's health and quality of life. The primary function of normal vascular endothelium is to function as a barrier function. However, in the presence of DM, glucose and lipid metabolism disorders, insulin resistance, inflammatory reactions, oxidative stress, and other factors cause vascular endothelial injury, leading to vascular endothelial lesions from morphology to function. Recently, numerous studies have found that autophagy plays a vital role in regulating the progression of vascular endothelial injury. Therefore, this article compares the morphology and function of normal and diabetic vascular endothelium and focuses on the current regulatory mechanisms and the important role of autophagy in diabetic vascular endothelial injury caused by different signal pathways. We aim to provide some references for future research on the mechanism of vascular endothelial injury in DM, investigate autophagy's protective or injurious effect, and study potential drugs using autophagy as a target.

Keywords: autophagy; diabetes; endothelial cells; pathological characteristics; vascular endothelial injury.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Display of morphological and structural abnormalities and the dysfunction of vascular endothelial injury in DM.
Figure 2
Figure 2
The classic autophagy activation pathway. MTORC1, rapamycin complex 1; ULK1/2, unc-51-like kinase 1/2; ATG, autophagy-related genes; RB1CC1, RB1-inducible coiled-coil 1; AMPK, AMP-activated protein kinase; BECN1, beclin 1; PIK3C3, phosphatidylinositol 3-kinase catalytic subunit type 3; PIK3R4, phosphoinositide 3-kinase regulatory subunit 4; AMBRA1, activating molecule in Beclin1-regulated autophagy protein 1; BCL2, B-cell lymphoma 2; ATG16L1, autophagy-related gene 16-like 1; LC3, microtubule-associated protein light chain 3; PE, phosphatidylethanolamine; SQSTM1, sequestosome 1; NBR1, neighbor of BRCA1 gene 1.
Figure 3
Figure 3
Autophagy is a balance to regulate vascular endothelial injury in DM from two different aspects.
See this image and copyright information in PMC

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