哺乳动物雷帕霉素靶蛋白通路在心肌细胞衰老引起心力衰竭中的研究进展

doi:10.12114/j.issn.1007-9572.2024.0650

中国全科医学 ›› 2026, Vol. 29 ›› Issue (36): 5452-5457.DOI: 10.12114/j.issn.1007-9572.2024.0650

所属专题：心力衰竭最新文章合辑

• 综述与专论 • 上一篇

哺乳动物雷帕霉素靶蛋白通路在心肌细胞衰老引起心力衰竭中的研究进展

王宇甲¹^,²^,³, 张金盈¹^,²^,³, 唐俊楠¹^,²^,³^,^*()

1．450052　河南省郑州市，郑州大学第一附属医院心血管内科
2．450052　河南省郑州市，河南省心脏损伤修复重点实验室
3．450052　河南省郑州市，河南省心血管疾病临床医学研究中心

收稿日期:2025-01-21 修回日期:2025-05-03 出版日期:2026-12-20 发布日期:2026-10-30
通讯作者: 唐俊楠
作者贡献：
王宇甲负责文章的构思与设计、论文撰写；张金盈、唐俊楠负责论文修订、文章的质量控制及审校。
基金资助:
国家自然科学基金资助项目(82222007, 82170281)

Research Progress of mTOR Pathway in Heart Failure Caused by Myocardial Aging

WANG Yujia¹^,²^,³, ZHANG Jinying¹^,²^,³, TANG Junnan¹^,²^,³^,^*()

1. Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China
2. Key Laboratory of Cardiac Injury and Repair of Henan Province, Zhengzhou 450052, China
3. Henan Province Clinical Research Center for Cardiovascular Diseases, Zhengzhou 450052, China

Received:2025-01-21 Revised:2025-05-03 Published:2026-12-20 Online:2026-10-30
Contact: TANG Junnan

摘要/Abstract

摘要： 心力衰竭是多种心脏疾病的终末期阶段，预后较差，其发病风险随年龄增长和心肌细胞衰老而显著增加。哺乳动物雷帕霉素靶蛋白（mTOR）通路在心肌细胞衰老的病理生理学中发挥关键作用。本文综述了mTOR通路在心肌细胞衰老引起心力衰竭中的最新研究进展，并探讨了延缓心肌细胞衰老的干预策略。心肌细胞衰老过程中mTOR复合物1（mTORC1）的持续激活通过调节蛋白质合成、脂质代谢和抑制自噬等机制，驱动心脏病理性改变并加速心力衰竭的发生、发展；而抑制mTORC1的过度激活能够延缓老年动物的心脏衰老进程并延长寿命。本文为缓解衰老引起的心力衰竭提供了新的见解，有助于减轻社会的疾病负担。

关键词: 心力衰竭, 心肌衰老, 哺乳动物雷帕霉素靶蛋白, 蛋白质合成, 脂代谢, 自噬

Abstract:

Heart failure is the end-stage of many heart diseases with poor prognosis, and its risk increases significantly with age and myocardial cell aging. The mammalian target of rapamycin (mTOR) pathway plays a key role in the pathophysiology of cardiomyocyte aging. This article reviews the latest research progress of the mTOR pathway in heart failure caused by myocardial cell aging, and explores potential intervention strategies to delay cardiomyocyte aging. This article shows that the continued activation of mTORC1 during aging drives pathological cardiac changes and accelerates the progression of heart failure by regulating protein synthesis, lipid metabolism, and inhibiting autophagy. Conversely, inhibiting the overactivation of mTORC1 can slow cardiac aging and extend lifespan in elderly animals. This article provides new insights into alleviating heart failure caused by aging and could help reduce the societal burden of this disease.

Key words: Heart failure, Cardiac aging, Mammalian target of rapamycin, Protein synthesis, Lipid metabolism, Autophagy

中图分类号:

R 541

王宇甲,张金盈,唐俊楠. 哺乳动物雷帕霉素靶蛋白通路在心肌细胞衰老引起心力衰竭中的研究进展[J]. 中国全科医学, 2026, 29(36): 5452-5457. DOI: 10.12114/j.issn.1007-9572.2024.0650.
WANG Yujia,ZHANG Jinying,TANG Junnan. Research Progress of mTOR Pathway in Heart Failure Caused by Myocardial Aging[J]. Chinese General Practice, 2026, 29(36): 5452-5457. DOI: 10.12114/j.issn.1007-9572.2024.0650.

参考文献 64

[1]	中国心血管健康与疾病报告编写组. 中国心血管健康与疾病报告2022概要[J]. 中国循环杂志, 2023, 38(6): 583-612. DOI: 10.3969/j.issn.1000-3614.2023.06.001.
[2]	Chen M S, Lee R T, Garbern J C. Senescence mechanisms and targets in the heart[J]. Cardiovasc Res, 2022, 118(5): 1173-1187. DOI: 10.1093/cvr/cvab161.
[3]	Triposkiadis F, Xanthopoulos A, Butler J. Cardiovascular aging and heart failure[J]. J Am Coll Cardiol, 2019, 74(6): 804-813. DOI: 10.1016/j.jacc.2019.06.053.
[4]	Kartha C C. Cardiomyocyte senescence[M]//Cardiomyocytes in Health and Disease. Cham: Springer International Publishing, 2021: 187-205. DOI: 10.1007/978-3-030-85536-9_12.
[5]	Takeuchi M, Kitano T, Nabeshima Y, et al. Left ventricular and left atrial volume ratio assessed by three-dimensional echocardiography: novel indices for evaluating age-related change in left heart chamber size[J]. Physiol Rep, 2019, 7(23): e14300. DOI: 10.14814/phy2.14300.
[6]	Ribeiro A S F, Zerolo B E, López-espuela F, et al. Cardiac system during the aging process[J]. Aging Dis, 2023, 14(4): 1105-1122. DOI: 10.14336/AD.2023.0115.
[7]	Sun S N, Ni S H, Li Y, et al. G-MDSCs promote aging-related cardiac fibrosis by activating myofibroblasts and preventing senescence[J]. Cell Death Dis, 2021, 12(6): 594. DOI: 10.1038/s41419-021-03874-7.
[8]	Lewandowski D, Yang E Y, Nguyen D T, et al. Relation of left ventricular diastolic function to global fibrosis burden: implications for heart failure risk stratification[J]. JACC Cardiovasc Imaging, 2023, 16(6): 783-796. DOI: 10.1016/j.jcmg.2022.12.027.
[9]	Leyva F, Zegard A, Okafor O, et al. Myocardial fibrosis predicts ventricular arrhythmias and sudden death after cardiac electronic device implantation[J]. J Am Coll Cardiol, 2022, 79(7): 665-678. DOI: 10.1016/j.jacc.2021.11.050.
[10]	Severino P, D'Amato A, Pucci M, et al. Ischemic heart disease and heart failure: role of coronary ion channels[J]. Int J Mol Sci, 2020, 21(9): 3167. DOI: 10.3390/ijms21093167.
[11]	Zhan Q Y, Peng W J, Wang S Q, et al. Heart failure with preserved ejection fraction: pathogenesis, diagnosis, exercise, and medical therapies[J]. J Cardiovasc Transl Res, 2023, 16(2): 310-326. DOI: 10.1007/s12265-022-10324-y.
[12]	Wang Y M, Vandewalle N, De Veirman K, et al. Targeting mTOR signaling pathways in multiple myeloma: biology and implication for therapy[J]. Cell Commun Signal, 2024, 22(1): 320. DOI: 10.1186/s12964-024-01699-3.
[13]	Proud C G, Xie J L. Regulation \| mTOR and its substrates[M]//Encyclopedia of Biological ChemistryⅢ. Amsterdam: Elsevier, 2021: 614-630. DOI: 10.1016/b978-0-12-819460-7.00001-3.
[14]	Dai D F, Kang P, Bai H. The mTOR signaling pathway in cardiac aging[J]. J Cardiovasc Aging, 2023, 3(3): 24. DOI: 10.20517/jca.2023.10.
[15]	Fu W X, Hall M N. Regulation of mTORC2 signaling[J]. Genes, 2020, 11(9): 1045. DOI: 10.3390/genes11091045.
[16]	Yoon M S. The role of mammalian target of rapamycin(mTOR)in insulin signaling[J]. Nutrients, 2017, 9(11): 1176. DOI: 10.3390/nu9111176.
[17]	Wang B, Jie Z L, Joo D, et al. TRAF2 and OTUD7B govern a ubiquitin-dependent switch that regulates mTORC2 signalling[J]. Nature, 2017, 545(7654): 365-369. DOI: 10.1038/nature22344.
[18]	Wang F J, Meng M, Mo B H, et al. Crosstalks between mTORC1 and mTORC2 variagate cytokine signaling to control NK maturation and effector function[J]. Nat Commun, 2018, 9(1): 4874. DOI: 10.1038/s41467-018-07277-9.
[19]	Ali E S, Mitra K, Akter S, et al. Recent advances and limitations of mTOR inhibitors in the treatment of cancer[J]. Cancer Cell Int, 2022, 22(1): 284. DOI: 10.1186/s12935-022-02706-8.
[20]	Xu W T, Chen H H, Xiao H Y. mTORC2: a neglected player in aging regulation[J]. J Cell Physiol, 2024, 239(11): e31363. DOI: 10.1002/jcp.31363.
[21]	Ballesteros-Álvarez J, Andersen J K. mTORC2: The other mTOR in autophagy regulation[J]. Aging Cell, 2021, 20(8): e13431. DOI: 10.1111/acel.13431.
[22]	Sato H, Leonardi M L, Roberti S L, et al. Maternal diabetes increases FOXO1 activation during embryonic cardiac development[J]. Mol Cell Endocrinol, 2023, 575: 111999. DOI: 10.1016/j.mce.2023.111999.
[23]	Zhang S J, Wang Y C, Yu M, et al. Discovery of herbacetin as a novel SGK1 inhibitor to alleviate myocardial hypertrophy[J]. Adv Sci, 2022, 9(2): e2101485. DOI: 10.1002/advs.202101485.
[24]	Sciarretta S, Forte M, Frati G, et al. New insights into the role of mTOR signaling in the cardiovascular system[J]. Circ Res, 2018, 122(3): 489-505. DOI: 10.1161/CIRCRESAHA.117.311147.
[25]	Mota-Martorell N, Jove M, Pradas I, et al. Gene expression and regulatory factors of the mechanistic target of rapamycin(mTOR)complex 1 predict mammalian longevity[J]. Geroscience, 2020, 42(4): 1157-1173. DOI: 10.1007/s11357-020-00210-3.
[26]	Blagosklonny M V. Cell senescence, rapamycin and hyperfunction theory of aging[J]. Cell Cycle, 2022, 21(14): 1456-1467. DOI: 10.1080/15384101.2022.2054636.
[27]	Daneshgar N, Rabinovitch P S, Dai D F. TOR signaling pathway in cardiac aging and heart failure[J]. Biomolecules, 2021, 11(2): 168. DOI: 10.3390/biom11020168.
[28]	Takahara T, Amemiya Y, Sugiyama R, et al. Amino acid-dependent control of mTORC1 signaling: a variety of regulatory modes[J]. J Biomed Sci, 2020, 27(1): 87. DOI: 10.1186/s12929-020-00679-2.
[29]	Candiracci J, Migeot V, Chionh Y H, et al. Reciprocal regulation of TORC signaling and tRNA modifications by Elongator enforces nutrient-dependent cell fate[J]. Sci Adv, 2019, 5(6): eaav0184. DOI: 10.1126/sciadv.aav0184.
[30]	Chiu H, Jackson L V, Oh K I, et al. The mTORC1/4E-BP/eIF4E axis promotes antibody class switching in B lymphocytes[J]. J Immunol, 2019, 202(2): 579-590. DOI: 10.4049/jimmunol.1800602.
[31]	Wang Y, Liao H J, Wang Y H, et al. KLK11 promotes the activation of mTOR and protein synthesis to facilitate cardiac hypertrophy[J]. BMC Cardiovasc Disord, 2021, 21(1): 266. DOI: 10.1186/s12872-021-02053-y.
[32]	Jiang X Y, Guan F F, Ma J X, et al. Cardiac-specific Trim44 knockout in rat attenuates isoproterenol-induced cardiac remodeling via inhibition of AKT/mTOR pathway[J]. Dis Model Mech, 2023, 16(5): dmm049444. DOI: 10.1242/dmm.049444.
[33]	Leggat J, Bidault G, Vidal-Puig A. Lipotoxicity: a driver of heart failure with preserved ejection fraction?[J]. Clin Sci, 2021, 135(19): 2265-2283. DOI: 10.1042/CS20210127.
[34]	Vaidyanathan S, Salmi T M, Sathiqu R M, et al. YAP regulates an SGK1/mTORC1/SREBP-dependent lipogenic program to support proliferation and tissue growth[J]. Dev Cell, 2022, 57(6): 719-731.e8. DOI: 10.1016/j.devcel.2022.02.004.
[35]	Lin J Y, Fan L L, Han Y M, et al. The mTORC1/eIF4E/HIF-1α pathway mediates glycolysis to support brain hypoxia resistance in the Gansu zokor, Eospalax cansus[J]. Front Physiol, 2021, 12: 626240. DOI: 10.3389/fphys.2021.626240.
[36]	Nacarelli T, Azar A, Altinok O, et al. Rapamycin increases oxidative metabolism and enhances metabolic flexibility in human cardiac fibroblasts[J]. Geroscience, 2018, 40(3): 243-256. DOI: 10.1007/s11357-018-0030-2.
[37]	Soliman G A, Acosta-Jaquez H A, Fingar D C. mTORC1 inhibition via rapamycin promotes triacylglycerol lipolysis and release of free fatty acids in 3T3-L1 adipocytes[J]. Lipids, 2010, 45(12): 1089-1100. DOI: 10.1007/s11745-010-3488-y.
[38]	Miyamoto S. Autophagy and cardiac aging[J]. Cell Death Differ, 2019, 26(4): 653-664. DOI: 10.1038/s41418-019-0286-9.
[39]	Dossou A S, Basu A. The emerging roles of mTORC1 in macromanaging autophagy[J]. Cancers, 2019, 11(10): 1422. DOI: 10.3390/cancers11101422.
[40]	Yang C L, Wang X C. Lysosome biogenesis: regulation and functions[J]. J Cell Biol, 2021, 220(6): e202102001. DOI: 10.1083/jcb.202102001.
[41]	Martina J A, Diab H I, Li L S, et al. The nutrient-responsive transcription factor TFE3 promotes autophagy, lysosomal biogenesis, and clearance of cellular debris[J]. Sci Signal, 2014, 7(309): ra9. DOI: 10.1126/scisignal.2004754.
[42]	Ramos F J, Chen S C, Garelick M G, et al. Rapamycin reverses elevated mTORC1 signaling in lamin A/C-deficient mice, rescues cardiac and skeletal muscle function, and extends survival[J]. Sci Transl Med, 2012, 4(144): 144ra103. DOI: 10.1126/scitranslmed.3003802.
[43]	Chang K, Kang P, Liu Y, et al. TGFB-INHB/activin signaling regulates age-dependent autophagy and cardiac health through inhibition of MTORC2[J]. Autophagy, 2020, 16(10): 1807-1822. DOI: 10.1080/15548627.2019.1704117.
[44]	Aspernig H, Heimbucher T, Qi W J, et al. Mitochondrial perturbations couple mTORC2 to autophagy in C. elegans[J]. Cell Rep, 2019, 29(6): 1399-1409.e5. DOI: 10.1016/j.celrep.2019.09.072.
[45]	Maestro I, Boya P, Martinez A. Serum- and glucocorticoid-induced kinase 1, a new therapeutic target for autophagy modulation in chronic diseases[J]. Expert Opin Ther Targets, 2020, 24(3): 231-243. DOI: 10.1080/14728222.2020.1730328.
[46]	Liu P D, Chang K, Requejo G, et al. mTORC2 protects the heart from high-fat diet-induced cardiomyopathy through mitochondrial fission in Drosophila[J]. Front Cell Dev Biol, 2022, 10: 866210. DOI: 10.3389/fcell.2022.866210.
[47]	Hsiao W Y, Jung S M, Tang Y F, et al. The lipid handling capacity of subcutaneous fat is programmed by mTORC2 during development[J]. Cell Rep, 2020, 33(1): 108223. DOI: 10.1016/j.celrep.2020.108223.
[48]	Zhang L L, Li Y Q, Wang Y, et al. mTORC2 facilitates liver regeneration through sphingolipid-induced PPAR-α-fatty acid oxidation[J]. Cell Mol Gastroenterol Hepatol, 2022, 14(6): 1311-1331. DOI: 10.1016/j.jcmgh.2022.07.011.
[49]	Guri Y, Colombi M, Dazert E, et al. mTORC2 promotes tumorigenesis via lipid synthesis[J]. Cancer Cell, 2017, 32(6): 807-823.e12. DOI: 10.1016/j.ccell.2017.11.011.
[50]	Lamming D W. Diminished mTOR signaling: a common mode of action for endocrine longevity factors[J]. Springerplus, 2014, 3: 735. DOI: 10.1186/2193-1801-3-735.
[51]	Arriola Apelo S I, Lin A, Brinkman J A, et al. Ovariectomy uncouples lifespan from metabolic health and reveals a sex-hormone-dependent role of hepatic mTORC2 in aging[J]. eLife, 2020, 9: e56177. DOI: 10.7554/eLife.56177.
[52]	Mulder F V M, Peeters E F H I, Westerink J, et al. The long-term effect of mTOR inhibition on lipid and glucose metabolism in tuberous sclerosis complex: data from the Dutch TSC registry[J]. Orphanet J Rare Dis, 2022, 17(1): 252. DOI: 10.1186/s13023-022-02385-8.
[53]	Schreiber K H, Arriola Apelo S I, Yu D Y, et al. A novel rapamycin analog is highly selective for mTORC1 in vivo[J]. Nat Commun, 2019, 10(1): 3194. DOI: 10.1038/s41467-019-11174-0.
[54]	Chakraborty A D, Kooiker K, Kobak K A, et al. Late-life rapamycin treatment enhances cardiomyocyte relaxation kinetics and reduces myocardial stiffness[J]. bioRxiv, 2023: 2023.06.12.544619. DOI: 10.1101/2023.06.12.544619.
[55]	Mannick J B, Lamming D W. Targeting the biology of aging with mTOR inhibitors[J]. Nat Aging, 2023, 3(6): 642-660. DOI: 10.1038/s43587-023-00416-y.
[56]	Kim S S, Lee C K. Growth signaling and longevity in mouse models[J]. BMB Rep, 2019, 52(1): 70-85. DOI: 10.5483/BMBRep.2019.52.1.299.
[57]	Kraig E, Linehan L A, Liang H Y, et al. A randomized control trial to establish the feasibility and safety of rapamycin treatment in an older human cohort: immunological, physical performance, and cognitive effects[J]. Exp Gerontol, 2018, 105: 53-69. DOI: 10.1016/j.exger.2017.12.026.
[58]	Boyalla V, Gallego-Colon E, Spartalis M. Immunity and inflammation in cardiovascular disorders[J]. BMC Cardiovasc Disord, 2023, 23(1): 148. DOI: 10.1186/s12872-023-03185-z.
[59]	Carrasco E, Gómez de Las Heras M M, Gabandé-rodríguez E, et al. The role of T cells in age-related diseases[J]. Nat Rev Immunol, 2022, 22(2): 97-111. DOI: 10.1038/s41577-021-00557-4.
[60]	Garza-Lombó C, Schroder A, Reyes-Reyes E M, et al. mTOR/AMPK signaling in the brain: cell metabolism, proteostasis and survival[J]. Curr Opin Toxicol, 2018, 8: 102-110. DOI: 10.1016/j.cotox.2018.05.002.
[61]	Fulton T L, Mirth C K, Piper M D W. Restricting a single amino acid cross-protects drosophila melanogaster from nicotine poisoning through mTORC1 and GCN2 signalling[J]. Open Biol, 2022, 12(12): 220319. DOI: 10.1098/rsob.220319.
[62]	Mattison J A, Colman R J, Beasley T M, et al. Caloric restriction improves health and survival of Rhesus monkeys[J]. Nat Commun, 2017, 8: 14063. DOI: 10.1038/ncomms14063.
[63]	Guo J, Huang X Q, Dou L, et al. Aging and aging-related diseases: from molecular mechanisms to interventions and treatments[J]. Signal Transduct Target Ther, 2022, 7(1): 391. DOI: 10.1038/s41392-022-01251-0.
[64]	James D L, Hawley N A, Mohr A E, et al. Impact of intermittent fasting and/or caloric restriction on aging-related outcomes in adults: a scoping review of randomized controlled trials[J]. Nutrients, 2024, 16(2): 316. DOI: 10.3390/nu16020316.

哺乳动物雷帕霉素靶蛋白通路在心肌细胞衰老引起心力衰竭中的研究进展

Research Progress of mTOR Pathway in Heart Failure Caused by Myocardial Aging

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