线粒体动力学与糖尿病并发症发病机制

郑宏庭; 瞿华

doi:10.16016/j.1000-5404.202111211

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线粒体动力学与糖尿病并发症发病机制

临床医学 | 更新时间：2026-01-09

- 线粒体动力学与糖尿病并发症发病机制
- Mitochondrial dynamics in the pathogenesis of diabetic complications
- 陆军军医大学学报 2022年44卷第1期页码：64-68
- 作者机构：
  
  400037 重庆，陆军军医大学（第三军医大学）第二附属医院内分泌科
- 作者简介：
  
  [郑宏庭，博士，主任医师，教授，博士研究生导师。国家杰出青年基金获得者，重庆市高校创新群体负责人，重庆市学术技术带头人，中央保健会诊专家。被评为军队高层次科技创新人才、全军与重庆市优秀博士生导师、军队院校育才银奖，为军队优秀专业技术人才一类岗位津贴获得者、陆军科技英才。担任中华医学会内分泌学分会全国委员、中国医师协会内分泌代谢科医师分会全国委员；JCEM、《第三军医大学学报》《中华内分泌代谢杂志》等期刊编委。主持国家杰出青年科学基金等各类科研课题20余项。获2019年度重庆市科技进步一等奖（排名第一）。以通讯作者在Sci Transl Med、Trends Endocrin Met、EMBO Mol Med、Hepatology、Diabetes等SCI收录期刊发表论文60余篇。主要从事线粒体稳态与糖尿病并发症基础与临床转化研究。E-mail: fnf7703@hotmail.com ZHENG Hongting, E-mail: fnf7703@hotmail.com
  [瞿华，博士，副主任医师，副教授，硕士研究生导师。主要从事线粒体稳态与糖尿病并发症基础与临床转化研究。E-mail: quhuahua120@163.com QU Hua, E-mail: quhuahua120@163.com
- 基金信息：
  
  国家自然科学基金杰青项目(81925007);国家自然科学基金面上项目(82070836)
- DOI：10.16016/j.1000-5404.202111211
  中图分类号： R329.24;R363.21;R587.2
- 收稿：2021-11-29，
  
  修回：2021-12-15，
  
  纸质出版：2022-01-15
- 稿件说明：
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郑宏庭, 瞿华. 线粒体动力学与糖尿病并发症发病机制[J]. 陆军军医大学学报, 2022,44(1):64-68.

Hongting ZHENG, Hua QU. Mitochondrial dynamics in the pathogenesis of diabetic complications[J]. Journal of Army Medical University, 2022, 44(1): 64-68.
郑宏庭, 瞿华. 线粒体动力学与糖尿病并发症发病机制[J]. 陆军军医大学学报, 2022,44(1):64-68. DOI： 10.16016/j.1000-5404.202111211.

Hongting ZHENG, Hua QU. Mitochondrial dynamics in the pathogenesis of diabetic complications[J]. Journal of Army Medical University, 2022, 44(1): 64-68. DOI： 10.16016/j.1000-5404.202111211.

摘要

线粒体动力学（mitochondrial dynamics）即线粒体融合与分裂保持动态平衡的过程。近年来的研究报道，这种动态变化在调控线粒体形态与数量、线粒体氧化代谢、膜电位及能量生成等方面发挥至关重要的作用。当人体罹患糖尿病时，高血糖可显著干扰线粒体融合与分裂的平衡态，影响线粒体数量、形态与功能，最终与多种糖尿病慢性并发症密切相关，但其具体机制尚不明确。本课题组长期致力于探究线粒体动力学在多种糖尿病并发症中的作用与机制。本文就线粒体动力学在糖尿病溃疡、糖尿病肾病以及糖尿病心肌病中的潜在机制及研究进展进行述评。

Abstract

Mitochondrial dynamics is the process of mitochondrial fusion and division to maintain dynamic balance. In recent years

it has been found that this dynamic change plays an important role in regulating mitochondrial morphology and quantity

mitochondrial oxidative metabolism

membrane potential and energy production. In diabetes

hyperglycemia significantly interferes with the dynamic balance of mitochondrial fusion and division process

and affects the quantity

morphology and function of mitochondria. And ultimately

the dynamic change of mitochondria is closely related to many chronic complications of diabetes

but the specific mechanism remains unclear. Our research group has long been committed to exploring the roles and mechanisms of mitochondrial dynamics in a variety of diabetic complications. This review summarizes the research progress and potential mechanisms of mitochondrial dynamics in diabetic ulcers

diabetic nephropathy and diabetic cardiomyopathy.

关键词

Keywords

references

WILLEMS P H, ROSSIGNOL R, DIETEREN C E, et al . Redox homeostasis and mitochondrial dynamics[J ] . Cell Metab, 2015, 22(2): 207-218. DOI: 10.1016/j.cmet.2015.06.006.

KOU Z Z, LI C Y, HU J C, et al . Alterations in the neural circuits from peripheral afferents to the spinal cord: possible implications for diabetic polyneuropathy in streptozotocin-induced type 1 diabetic rats[J ] . Front Neural Circuits, 2014, 8: 6. DOI: 10.3389/fncir.2014.00006.

WENG T Y, TSAI S A, SU T P. Roles of sigma-1 receptors on mitochondrial functions relevant to neurodegenerative diseases[J]. J Biomed Sci, 2017, 24(1): 74. DOI: 10.1186/s12929-017-0380-6.

RUEGSEGGER G N, CREO A L, CORTES T M, et al . Altered mitochondrial function in insulin-deficient and insulin-resistant states[J ] . J Clin Invest, 2018, 128(9): 3671-3681. DOI: 10.1172/jci120843.

PETERSEN K F, BEFROY D, DUFOUR S, et al . Mitochondrial dysfunction in the elderly: possible role in insulin resistance[J ] . Science, 2003, 300(5622): 1140-1142. DOI: 10.1126/science.1082889.

BOWLING F L, RASHID S T, BOULTON A J. Preventing and treating foot complications associated with diabetes mellitus[J]. Nat Rev Endocrinol, 2015, 11(10): 606-616. DOI: 10.1038/nrendo.2015.130.

KUNKEMOELLER B, KYRIAKIDES T R. Redox signaling in diabetic wound healing regulates extracellular matrix deposition[J]. Antioxid Redox Signal, 2017, 27(12): 823-838. DOI: 10.1089/ars.2017.7263.

TATMATSU-ROCHA J C, TIM C R, AVO L, et al . Mitochondrial dynamics (fission and fusion) and collagen production in a rat model of diabetic wound healing treated by photobiomodulation: comparison of 904 nm laser and 850 nm light-emitting diode (LED)[J ] . J Photochem Photobiol B, 2018, 187: 41-47. DOI: 10.1016/j.jphotobiol.2018.07.032.

KIM Y M, YOUN S W, SUDHAHAR V, et al . Redox regulation of mitochondrial fission protein Drp1 by protein disulfide isomerase limits endothelial senescence[J ] . Cell Rep, 2018, 23(12): 3565-3578. DOI: 10.1016/j.celrep.2018.05.054.

FU H Y, ZHOU H D, YU X H, et al . Wounding triggers MIRO-1 dependent mitochondrial fragmentation that accelerates epidermal wound closure through oxidative signaling[J ] . Nat Commun, 2020, 11(1): 1050. DOI: 10.1038/s41467-020-14885-x.

SU L N, ZHANG Y R, HE K C, et al . Activation of transient receptor potential vanilloid 1 accelerates re-endothelialization and inhibits neointimal formation after vascular injury[J ] . J Vasc Surg, 2017, 65(1): 197-205. e2. DOI: 10.1016/j.jvs.2015.12.037.

QU H, MIAO T, WANG Y R, et al . Dedicator of cytokinesis 5 regulates keratinocyte function and promotes diabetic wound healing[J ] . Diabetes, 2021, 70(5): 1170-1184. DOI: 10.2337/db20-1008.

THOMAS M C, COOPER M E, ZIMMET P. Changing epidemiology of type 2 diabetes mellitus and associated chronic kidney disease[J]. Nat Rev Nephrol, 2016, 12(2): 73-81. DOI: 10.1038/nrneph.2015.173.

GROSS J L, DE AZEVEDO M J, SILVEIRO S P, et al . Diabetic nephropathy: diagnosis, prevention, and treatment[J ] . Diabetes Care, 2005, 28(1): 164-176. DOI: 10.2337/diacare.28.1.164.

SUN L, XIE P, WADA J, et al . Rap1b GTPase ameliorates glucose-induced mitochondrial dysfunction[J ] . J Am Soc Nephrol, 2008, 19(12): 2293-2301. DOI: 10.1681/asn.2008030336.

ZHENG N, LIANG T, XU X H, et al . Polydatin impairs mitochondria fitness and ameliorates podocyte injury by suppressing Drp1 expression[J ] . J Cell Physiol, 2017, 232(10): 2776-2787. DOI: 10.1002/jcp.25943.

HIGGINS G C, COUGHLAN M T. Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy?[J]. Br J Pharmacol, 2014, 171(8): 1917-1942. DOI: 10.1111/bph.12503.

WANG W J, WANG Y, LONG J Y, et al . Mitochondrial fission triggered by hyperglycemia is mediated by ROCK1 activation in podocytes and endothelial cells[J ] . Cell Metab, 2012, 15(2): 186-200. DOI: 10.1016/j.cmet.2012.01.009.

SHEN L, ZHANG Q F, TU S M, et al . SIRT3 mediates mitofusin 2 ubiquitination and degradation to suppress ischemia reperfusion-induced acute kidney injury[J ] . Exp Cell Res, 2021, 408(2): 112861. DOI: 10.1016/j.yexcr.2021.112861.

CLEVELAND K H, BROSIUS F C 3rd, SCHNELLMANN R G. Regulation of mitochondrial dynamics and energetics in the diabetic renal proximal tubule by the β2-adrenergic receptor agonist formoterol[J]. Am J Physiol Renal Physiol, 2020, 319(5): F773-F779. DOI: 10.1152/ajprenal.00427.2020.

QU H, GONG X L, LIU X F, et al . Deficiency of mitochondrial glycerol 3-phosphate dehydrogenase exacerbates podocyte injury and the progression of diabetic kidney disease[J ] . Diabetes, 2021, 70(6): 1372-1387. DOI: 10.2337/db20-1157.

HTAY T, SOE K, LOPEZ-PEREZ A, et al . Mortality and cardiovascular disease in type 1 and type 2 diabetes[J ] . Curr Cardiol Rep, 2019, 21(6): 45. DOI: 10.1007/s11886-019-1133-9.

MAACK C, LEHRKE M, BACKS J, et al . Heart failure and diabetes: metabolic alterations and therapeutic interventions: a state-of-the-art review from the Translational Research Committee of the Heart Failure Association-European Society of Cardiology[J ] . Eur Heart J, 2018, 39(48): 4243-4254. DOI: 10.1093/eurheartj/ehy596.

MARWICK T H, RITCHIE R, SHAW J E, et al . Implications of underlying mechanisms for the recognition and management of diabetic cardiomyopathy[J ] . J Am Coll Cardiol, 2018, 71(3): 339-351. DOI: 10.1016/j.jacc.2017.11.019.

WU S N, LU Q L, DING Y, et al . Hyperglycemia-driven inhibition of AMP-activated protein kinase α2 induces diabetic cardiomyopathy by promoting mitochondria-associated endoplasmic reticulum membranes in vivo[J ] . Circulation, 2019, 139(16): 1913-1936. DOI: 10.1161/CIRCULATIONAHA.118.033552.

WATANABE T, SAOTOME M, NOBUHARA M, et al . Roles of mitochondrial fragmentation and reactive oxygen species in mitochondrial dysfunction and myocard ial insulin resistance[J ] . Exp Cell Res, 2014, 323(2): 314-325. DOI: 10.1016/j.yexcr.2014.02.027.

WU Q R, ZHENG D L, LIU P M, et al . High glucose induces Drp1-mediated mitochondrial fission via the Orai1 calcium channel to participate in diabetic cardiomyocyte hypertrophy[J ] . Cell Death Dis, 2021, 12(2): 216. DOI: 10.1038/s41419-021-03502-4.

WANG Y, WANG Y, LI F, et al . Spermine protects cardiomyocytes from high glucose-induced energy disturbance by targeting the CaSR-gp78-ubiquitin proteasome system[J ] . Cardiovasc Drugs Ther, 2021, 35(1): 73-85. DOI:10.1007/s10557-020-07064-z.

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