12
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Traditional Chinese medicine and its active substances reduce vascular injury in diabetes via regulating autophagic activity

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Due to its high prevalence, poor prognosis, and heavy burden on healthcare costs, diabetic vascular complications have become a significant public health issue. Currently, the molecular and pathophysiological mechanisms underlying diabetes-induced vascular complications remain incompletely understood. Autophagy, a highly conserved process of lysosomal degradation, maintains intracellular homeostasis and energy balance via removing protein aggregates, damaged organelles, and exogenous pathogens. Increasing evidence suggests that dysregulated autophagy may contribute to vascular abnormalities in various types of blood vessels, including both microvessels and large vessels, under diabetic conditions. Traditional Chinese medicine (TCM) possesses the characteristics of “multiple components, multiple targets and multiple pathways,” and its safety has been demonstrated, particularly with minimal toxicity in liver and kidney. Thus, TCM has gained increasing attention from researchers. Moreover, recent studies have indicated that Chinese herbal medicine and its active compounds can improve vascular damage in diabetes by regulating autophagy. Based on this background, this review summarizes the classification, occurrence process, and related molecular mechanisms of autophagy, with a focus on discussing the role of autophagy in diabetic vascular damage and the protective effects of TCM and its active compounds through the regulation of autophagy in diabetes. Moreover, we systematically elucidate the autophagic mechanisms by which TCM formulations, individual herbal extracts, and active compounds regulate diabetic vascular damage, thereby providing new candidate drugs for clinical treatment of vascular complications in diabetes. Therefore, further exploration of TCM and its active compounds with autophagy-regulating effects holds significant research value for achieving targeted therapeutic approaches for diabetic vascular complications.

          Related collections

          Most cited references126

          • Record: found
          • Abstract: found
          • Article: not found

          AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1.

          Autophagy is a process by which components of the cell are degraded to maintain essential activity and viability in response to nutrient limitation. Extensive genetic studies have shown that the yeast ATG1 kinase has an essential role in autophagy induction. Furthermore, autophagy is promoted by AMP activated protein kinase (AMPK), which is a key energy sensor and regulates cellular metabolism to maintain energy homeostasis. Conversely, autophagy is inhibited by the mammalian target of rapamycin (mTOR), a central cell-growth regulator that integrates growth factor and nutrient signals. Here we demonstrate a molecular mechanism for regulation of the mammalian autophagy-initiating kinase Ulk1, a homologue of yeast ATG1. Under glucose starvation, AMPK promotes autophagy by directly activating Ulk1 through phosphorylation of Ser 317 and Ser 777. Under nutrient sufficiency, high mTOR activity prevents Ulk1 activation by phosphorylating Ulk1 Ser 757 and disrupting the interaction between Ulk1 and AMPK. This coordinated phosphorylation is important for Ulk1 in autophagy induction. Our study has revealed a signalling mechanism for Ulk1 regulation and autophagy induction in response to nutrient signalling.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Autophagy: cellular and molecular mechanisms.

            Autophagy is a self-degradative process that is important for balancing sources of energy at critical times in development and in response to nutrient stress. Autophagy also plays a housekeeping role in removing misfolded or aggregated proteins, clearing damaged organelles, such as mitochondria, endoplasmic reticulum and peroxisomes, as well as eliminating intracellular pathogens. Thus, autophagy is generally thought of as a survival mechanism, although its deregulation has been linked to non-apoptotic cell death. Autophagy can be either non-selective or selective in the removal of specific organelles, ribosomes and protein aggregates, although the mechanisms regulating aspects of selective autophagy are not fully worked out. In addition to elimination of intracellular aggregates and damaged organelles, autophagy promotes cellular senescence and cell surface antigen presentation, protects against genome instability and prevents necrosis, giving it a key role in preventing diseases such as cancer, neurodegeneration, cardiomyopathy, diabetes, liver disease, autoimmune diseases and infections. This review summarizes the most up-to-date findings on how autophagy is executed and regulated at the molecular level and how its disruption can lead to disease. Copyright (c) 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis.

              Dysfunction of the endothelial lining of lesion-prone areas of the arterial vasculature is an important contributor to the pathobiology of atherosclerotic cardiovascular disease. Endothelial cell dysfunction, in its broadest sense, encompasses a constellation of various nonadaptive alterations in functional phenotype, which have important implications for the regulation of hemostasis and thrombosis, local vascular tone and redox balance, and the orchestration of acute and chronic inflammatory reactions within the arterial wall. In this review, we trace the evolution of the concept of endothelial cell dysfunction, focusing on recent insights into the cellular and molecular mechanisms that underlie its pivotal roles in atherosclerotic lesion initiation and progression; explore its relationship to classic, as well as more recently defined, clinical risk factors for atherosclerotic cardiovascular disease; consider current approaches to the clinical assessment of endothelial cell dysfunction; and outline some promising new directions for its early detection and treatment.
                Bookmark

                Author and article information

                Contributors
                Role: Role: Role:
                Role: Role: Role:
                Role: Role: Role: Role:
                Role: Role: Role:
                Role: Role: Role:
                Role: Role: Role: Role:
                Role: Role:
                URI : https://loop.frontiersin.org/people/2603577/overviewRole: Role: Role:
                Journal
                Front Pharmacol
                Front Pharmacol
                Front. Pharmacol.
                Frontiers in Pharmacology
                Frontiers Media S.A.
                1663-9812
                04 March 2024
                2024
                : 15
                : 1355246
                Affiliations
                [1] 1 Department of Basic Medicine , Gansu University of Traditional Chinese Medicine , Lanzhou, China
                [2] 2 Department of Traditional Chinese Medicine , Fujian University of Traditional Chinese Medicine , Lanzhou, China
                [3] 3 Department of Traditional Chinese Medicine , Jiangxi University of Traditional Chinese Medicine , Nanchang, China
                [4] 4 Department of Traditional Chinese Medicine , Ningxia Medical University , Yinchuan, China
                Author notes

                Edited by: Stalin Antony, University of Electronic Science and Technology of China, China

                Reviewed by: Shihan Wang, Guang’anmen Hospital, China

                Peizheng Yan, Shandong University of Traditional Chinese Medicine, China

                *Correspondence: Xiangdong Zhu, zhuxiangdong33@ 123456163.com ; Yonglin Liang, 875532437@ 123456qq.com
                [ † ]

                These authors have contributed equally to this work

                Article
                1355246
                10.3389/fphar.2024.1355246
                10949535
                38505420
                35a68216-a239-4f24-a55a-78076e9b71e5
                Copyright © 2024 Gao, Zhang, Zhang, Liu, Liu, Li, Zhu and Liang.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 13 December 2023
                : 26 February 2024
                Funding
                The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. This present study was supported by the National Natural Science Foundation of China, Grant/Award Number: 82360914, and the Gansu Provincial Department of Education Project, Grant/Award Number: 2021CYZC-03.
                Categories
                Pharmacology
                Review
                Custom metadata
                Ethnopharmacology

                Pharmacology & Pharmaceutical medicine
                diabetic vascular complications,autophagy,tcm formulations,herbal extracts,active compounds

                Comments

                Comment on this article