Research progress of succinate and atherosclerosis
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Affiliation:

1.Department of Cardiovascular Medicine, The Second Affiliated Hospital, University of South China, Hengyang, Hunan 421001, China;2.Institute of Cardiovascular Diseases, Hengyang Medical School, University of South China, Hengyang, Hunan 421001,China)

Clc Number:

R5

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    Abstract:

    Cardiovascular disease is the leading cause of death. Moreover, the incidence of cardiovascular disease in young/middle-aged people (18~45 years old) is still on the rise. Early diagnosis, early warning and treatment of cardiovascular disease are important topics in the current medical research field. Atherosclerosis is the pathophysiological basis of many cardiovascular diseases. Recent studies have shown that the tricarboxylic acid (TCA) cycle intermediate is involved in the occurrence and development of atherosclerosis, and considered as the early diagnosis and warning bio-markers for atherosclerosis. Here, the roles and underlying mechanisms of succinate in the initiation and progression in atherosclerosis were reviewed.

    Reference
    [1] 中国心血管健康与疾病报告2020编写组.《中国心血管健康与疾病报告2020》概述.中国心血管病研究,1,9(7):582-590.
    [2] AENGEVAEREN V L, MOSTERD A, SHARMA S, et al.Exercise and coronary atherosclerosis:observations, explanations, relevance, and clinical management.Circulation, 0,1(16):1338-1350.
    [3] MOUTON A J, LI X, HALL M E, et al.Obesity, hypertension, and cardiac dysfunction:novel roles of immunometabolism in macrophage activation and inflammation.Circ Res, 0,6(6):789-806.
    [4] FREMDER M, KIM S W, KHAMAYSI A, et al.A transepithelial pathway delivers succinate to macrophages, thus perpetuating their pro-inflammatory metabolic state.Cell Rep, 1,6(6):109521.
    [5] LU Y T, LI L Z, YANG Y L, et al.Succinate induces aberrant mitochondrial fission in cardiomyocytes through GPR91 signaling.Cell Death Dis, 8,9(6):672.
    [6] MA P, WANG Z, WANG Y, et al.Integration of metabolomics and transcriptomics reveals ketone body and lipid metabolism disturbance related to ER stress in the liver.J Proteome Res, 1,0(8):3875-3888.
    [7] OSUNA-PRIETO F J, MARTINEZ-TELLEZ B, ORTIZ-ALVAREZ L, et al.Elevated plasma succinate levels are linked to higher cardiovascular disease risk factors in young adults.Cardiovasc Diabetol, 1,0(1):151.
    [8] LIU B, LI J, LIN X, et al.The metabolic changes in the hippocampus of an atherosclerotic rat model and the regulation of aerobic training.Metab Brain Dis, 0,5(6):1017-1034.
    [9] CHOUCHANI E T, PELL V R, GAUDE E A, et al.Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS.Nature, 4,5(7527):431.
    [10] MURPHY M P, LAJ O.Krebs cycle reimagined:the emerging roles of succinate and itaconate as signal transducers.Cell, 8,4(4):780-784.
    [11] MARTIN J L, COSTA A, GRUSZCZYK A V, et al.Succinate accumulation drives ischaemia-reperfusion injury during organ transplantation.Nat Metab, 9,1:966-974.
    [12] MILLS E L, KELLY B, LOGAN A, et al.Repurposing mitochondria from ATP production to ROS generation drives a pro-inflammatory phenotype in macrophages that depends on succinate oxidation by complex Ⅱ.Cell, 6,7(2):457-470.
    [13] BURTENSHAW D, KITCHING M, REDMOND E M, et al.Reactive oxygen species (ROS), intimal thickening, and subclinical atherosclerotic disease.Front Cardiovasc Med, 9,6:89.
    [14] MARCHIO P, GUERRA-OJEDA S, VILA J M, et al.Targeting early atherosclerosis:a focus on oxidative stress and inflammation.Oxid Med Cell Longev, 9,9:8563845.
    [15] MERCER J R, YU E, FIGG N, et al.The mitochondria-targeted antioxidant MitoQ decreases features of the metabolic syndrome in ATM+/-/ApoE-/- mice.Free Radic Biol Med, 2,2(5):841-849.
    [16] WANG Y, LI L, ZHAO W, et al.Targeted therapy of atherosclerosis by a broad-spectrum reactive oxygen species scavenging nanoparticle with intrinsic anti-inflammatory activity.ACS Nano, 8,2(9):8943-8960.
    [17] LECCE L, XU Y, V'GANGULA B, et al.Histone deacetylase 9 promotes endothelial-mesenchymal transition and an unfavorable atherosclerotic plaque phenotype.J Clin Invest, 1,1(15):e131178.
    [18] SUN H J, WU Z Y, NIE X W, et al.Role of endothelial dysfunction in cardiovascular diseases:the Link between inflammation and Hydrogen sulfide.Front Pharmacol, 9,0:1568.
    [19] 章舒蕾, 梁亚敏, 罗涔方, 等.琥珀酸通过活性氧途径诱导人脐静脉内皮细胞焦亡.中国动脉硬化杂志, 1,9(1):42-47.
    [20] HE B, NIE Q, WANG F, et al.Role of pyroptosis in atherosclerosis and its therapeutic implications.J Cell Physiol, 1,6(10):7159-7175.
    [21] 曹朝晖, 吴颛, 胡小波.细胞焦亡参与动脉粥样硬化形成的分子机制新进展.中国动脉硬化杂志, 1,9(7):560-565.
    [22] CHEN J, ZHANG J, WU J, et al.Low shear stress induced vascular endothelial cell pyroptosis by TET2/SDHB/ROS pathway.Free Radic Biol Med, 1,2:582-591.
    [23] WU P, CHEN J N, CHEN J J, et al.Trimethylamine N-oxide promotes ApoE-/- mice atherosclerosis by inducing vascular endothelial cell pyroptosis via the SDHB/ROS pathway.J Cell Physiol, 0,5(10):6582-6591.
    [24] ZHANG H, ZHENG J, LIN J, et al.miR-758 mediates oxLDL-dependent vascular endothelial cell damage by suppressing the succinate receptor SUCNR1.Gene, 8,3:1-8.
    [25] NEWSHOLME P, CURI R, GORDON S, et al.Metabolism of glucose, glutamine, long-chain fatty acids and ketone bodies by murine macrophages.Biochem J, 6,9(1):121-125.
    [26] PALMIER E M, MENGA A, MARTIN-PEREZ R, et al.Pharmacologic or genetic targeting of glutamine synthetase skews macrophages toward an M1-like phenotype and inhibits tumor metastasis.Cell Rep, 7,0(7):1654-1666.
    [27] KOENIS D S, MEDZIKOVIC L, VAN LOENEN P B, et al.Nuclear receptor Nur77 limits the macrophage inflammatory response through transcriptional reprogramming of mitochondrial metabolism.Cell Rep, 8,4(8):2127-2140.e7.
    [28] LE C T, NGUYEN G, PARK S Y, et al.LY2405319, an analog of fibroblast growth factor 21 ameliorates α-smooth muscle actin production through inhibition of the succinate-G-protein couple receptor 91 (GPR91) pathway in mice.PLoS One, 8,3(2):e0192146.
    [29] WANG Z, CHEN L, HUANG Y, et al.Pharmaceutical targeting of succinate dehydrogenase in fibroblasts controls bleomycin-induced lung fibrosis.Redox Biol, 1,6:102082.
    [30] HENDERSON J, DUFFY L, STRATTON R, et al.Metabolic reprogramming of glycolysis and glutamine metabolism are key events in myofibroblast transition in systemic sclerosis pathogenesis.J Cell Mol Med, 0,4(23):14026-14038.
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ZENG Yan, WEI Dangheng, ZENG Gaofeng. Research progress of succinate and atherosclerosis[J]. Editorial Office of Chinese Journal of Arteriosclerosis,2022,30(1):83-87.

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History
  • Received:September 26,2021
  • Revised:November 28,2021
  • Online: January 07,2022
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