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中华老年病研究电子杂志 ›› 2026, Vol. 13 ›› Issue (02) : 44 -52. doi: 10.3877/cma.j.issn.2095-8757.2026.02.007

综述

衰老性骨病与心血管疾病共病机制研究进展
周志豪1, 沈国灿1, 成艳美2, 张晓芳3, 王景浩3, 王志国3, 王华军1, 郑小飞1,()   
  1. 1510630 广州,暨南大学附属第一医院运动医学科
    3510630 广州,暨南大学附属第一医院药学部
    2510080 广州,中山大学附属第一医院心胸外科ICU
  • 收稿日期:2026-01-23 出版日期:2026-05-28
  • 通信作者: 郑小飞
  • 基金资助:
    国家重点研发计划"诊疗装备与生物医用材料"重点专项项目(2023YFC2414500); 广州市校(院)企联合资助项目(2024A03J0971); 暨南大学医学联合基金"临床医学+X"交叉揭榜挂帅项目(YXJC2022005); 广东省速度能力研究重点实验室开放基金资助项目(2023B1212010009); 暨南大学附属第一医院临床前沿新技术项目(No. JNU1AF-CFTP-2022-a01204)

Research advances in comorbid mechanisms linking age-related bone disease and cardiovascular disease

Zhihao Zhou1, Guocan Shen1, Yanmei Cheng2, Xiaofang Zhang3, Jinghao Wang3, Zhiguo Wang3, Huajun Wang1, Xiaofei Zheng1,()   

  1. 1Department of Sports Medicine, The First Affiliated Hospital of Jinan University, Guangzhou 510630, China
    3Department of Pharmacy, The First Affiliated Hospital of Jinan University, Guangzhou 510630, China
    2Department of Cardiothoracic Surgery ICU, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China
  • Received:2026-01-23 Published:2026-05-28
  • Corresponding author: Xiaofei Zheng
引用本文:

周志豪, 沈国灿, 成艳美, 张晓芳, 王景浩, 王志国, 王华军, 郑小飞. 衰老性骨病与心血管疾病共病机制研究进展[J/OL]. 中华老年病研究电子杂志, 2026, 13(02): 44-52.

Zhihao Zhou, Guocan Shen, Yanmei Cheng, Xiaofang Zhang, Jinghao Wang, Zhiguo Wang, Huajun Wang, Xiaofei Zheng. Research advances in comorbid mechanisms linking age-related bone disease and cardiovascular disease[J/OL]. Chinese Journal of Geriatrics Research(Electronic Edition), 2026, 13(02): 44-52.

衰老性骨病(如骨关节炎、骨质疏松症)与心血管疾病(如高血压、动脉粥样硬化、心房颤动及心力衰竭)是老年人群中常见的慢性疾病。近年来,流行病学研究提示,骨关节炎、骨质疏松症患者心血管事件风险可能升高,而心血管疾病患者亦可伴随骨量下降、骨微结构破坏或关节退变加重,但两者之间的因果方向和具体机制关联尚未完全明确。现有研究表明,炎性衰老、氧化应激、内分泌紊乱、矿物质代谢异常、代谢重编程、自噬功能下降及细胞外基质重塑等过程,可能共同参与骨骼、关节、血管和心脏组织的病理改变。此文从共同危险因素与衰老相关基础机制、具体疾病间的交互机制两个层面,系统综述衰老性骨病与心血管疾病共病机制的研究进展,并对现有证据的局限性及潜在临床转化价值进行评述,以期为骨病与心血管疾病综合管理策略优化提供参考。

Aging-related bone disease (e.g., osteoarthritis and osteoporosis) and cardiovascular disease (e.g., hypertension, atherosclerosis, atrial fibrillation, and heart failure) are common chronic degenerative disease in the elderly population. In recent years, epidemiological studies have suggested that patients with osteoarthritis or osteoporosis may have an increased risk of cardiovascular events, while patients with cardiovascular disease may also exhibit bone loss, deterioration of bone microarchitecture, or aggravated joint degeneration. However, the causal direction and specific mechanistic links between these conditions remain incompletely defined. Current evidence indicates that inflammaging, oxidative stress, endocrine dysregulation, disordered mineral metabolism, metabolic reprogramming, impaired autophagy, and extracellular matrix remodeling may collectively contribute to pathological changes in bone, joint, vascular, and cardiac tissues. This review systematically summarizes recent advances in the comorbidity between aging-related bone disease and cardiovascular disease from two perspectives: shared risk factors and fundamental aging-related mechanisms, and disease-specific crosstalk mechanisms. It also discusses the limitations of existing evidence and the potential clinical translational value of this field, aiming to provide a reference for mechanistic research on bone-cardiovascular comorbidity and the optimization of integrated management strategies.

[1]
Boutet MA, Nerviani A, Fossati-Jimack L, et al. Comparative analysis of late-stage rheumatoid arthritis and osteoarthritis reveals shared histopathological features[J]. Osteoarthritis Cartilage, 2024, 32(2):166-176.
[2]
国家心血管病中心,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2023概要[J].中国循环杂志202439(7):625-660.
[3]
Yu F, Xia W. The epidemiology of osteoporosis, associated fragility fractures, and management gap in China[J]. Arch Osteoporos, 2019, 14(1):32.
[4]
Pan XB, Ma QY, Gao T, et al. Osteoporosis risk and its association with all-cause and cause-specific mortality among the elderly: A 16-year nationwide cohort study [J]. BMC Geriatr, 2025, 25(1):199.
[5]
Pan J, Zou Y, Zhang Q, et al. Mortality risk in osteoarthritis patients: A meta-analysis of observational studies[J]. BMC Musculoskelet Disord, 2025, 26(1):1102.
[6]
Wright VJ, Schwartzman JD, Itinoche R, et al. The musculoskeletal syndrome of menopause[J]. Climacteric, 2024, 27(5):466-472.
[7]
Wu X, Zhang M. Effects of androgen and progestin on the proliferation and differentiation of osteoblasts[J]. Exp Ther Med, 2018, 16(6):4722-4728.
[8]
Deng C, Presle N, Pizard A, et al. Beneficial impact of eicosapentaenoic acid on the adverse effects induced by palmitate and hyperglycemia on healthy rat chondrocyte[J]. Int J Mol Sci, 2024, 25(3):1810.
[9]
Engin A. Reappraisal of adipose tissue inflammation in obesity[J]. Adv Exp Med Biol, 2024, 1460:297-327.
[10]
Zhang S, Hao W, Chen D, et al. Intermittent administration of PTH for the treatment of inflammatory bone loss does not enhance entheseal pathological new bone formation[J]. Biochem Biophys Res Commun, 2024, 711:149888.
[11]
Torremadé N, Bozic M, Panizo S, et al. Vascular calcification induced by chronic kidney disease is mediated by an increase of 1α-hydroxylase expression in vascular smooth muscle cells [J]. J Bone Miner Res, 2016, 31(10):1865-1876.
[12]
De La Guía-Galipienso F, Martínez-Ferran M, Vallecillo N, et al. Vitamin D and cardiovascular health[J]. Clin Nutr, 2021, 40(5):2946-2957.
[13]
Zhang HN, Xu QQ, Thakur A, et al. Endothelial dysfunction in diabetes and hypertension: Role of microRNAs and long non-coding RNAs[J]. Life Sci, 2018, 213:258-268.
[14]
Li Q, Fu J, Park K, et al. Insulin receptors in vascular smooth muscle cells regulate plaque stability of atherosclerosis[J]. Cardiovasc Res, 2024, 120(16):2017-2030.
[15]
Guo X, Liu S, Wu X, et al. Alleviating vascular calcification with Bushen Huoxue formula in rats with chronic kidney disease by inhibiting the PTEN/PI3K/AKT signaling pathway through exosomal microRNA-32[J]. J Pharm Pharmacol, 2025, 77(4):550-563.
[16]
Zuccolo E, Badi I, Scavello F, et al. The microRNA-34a-Induced senescence-associated secretory phenotype (sasp) favors vascular smooth muscle cells calcification[J]. Int J Mol Sci, 2020, 21(12):4454.
[17]
Catheline SE, Bell RD, Oluoch LS, et al. IKKβ-NF-κB signaling in adult chondrocytes promotes the onset of age-related osteoarthritis in mice[J]. Sci Signal, 2021, 14(701):eabf3535.
[18]
Fang G, Li X, Yang F, et al. Amentoflavone mitigates doxorubicin-induced cardiotoxicity by suppressing cardiomyocyte pyroptosis and inflammation through inhibition of the STING/NLRP3 signalling pathway[J]. Phytomedicine, 2023, 117:154922.
[19]
Sun S, Ji Z, Fu J, et al. Endosulfan induces endothelial inflammation and dysfunction via IRE1α/NF-κB signaling pathway[J]. Environ Sci Pollut Res Int, 2020, 27(21):26163-26171.
[20]
Hussain S, Sun M, Guo Y, et al. SFMBT2 positively regulates SOX9 and chondrocyte proliferation[J]. Int J Mol Med, 2018, 42(6):3503-3512.
[21]
Sproston NR, Ashworth JJ. Role of C-Reactive Protein at Sites of Inflammation and Infection[J]. Front Immunol, 2018, 9:754.
[22]
Li R, Kato H, Fumimoto C, et al. Essential amino acid starvation-induced oxidative stress causes DNA damage and apoptosis in murine osteoblast-like cells[J]. Int J Mol Sci, 2023, 24(20):15314.
[23]
Morgan MJ, Liu ZG. Crosstalk of reactive oxygen species and NF-κB signaling[J]. Cell Res, 2011, 21(1):103-115.
[24]
Shimura D, Shaw RM. GJA1-20k and mitochondrial dynamics[J]. Front Physiol, 2022, 13:867358.
[25]
Liu L, Zhang W, Liu T, et al. The physiological metabolite α-ketoglutarate ameliorates osteoarthritis by regulating mitophagy and oxidative stress[J]. Redox Biol, 2023, 62:102663.
[26]
Lee WC, Guntur AR, Long F, et al. Energy metabolism of the osteoblast: Implications for osteoporosis[J]. Endocr Rev, 2017, 38(3):255-266.
[27]
Li X, Chen M, Chen X, et al. TRAP1 drives smooth muscle cell senescence and promotes atherosclerosis via HDAC3-primed histone H4 lysine 12 lactylation[J]. Eur Heart J, 2024, 45(39):4219-4235.
[28]
Kalucka J, Bierhansl L, Conchinha NV, et al. Quiescent endothelial cells upregulate fatty acid β-oxidation for vasculoprotection via redox homeostasis[J]. Cell Metab, 2018, 28(6):881-894.
[29]
Tyrrell DJ, Blin MG, Song J, et al. Age-associated mitochondrial dysfunction accelerates atherogenesis[J]. Circ Res, 2020, 126(3):298-314.
[30]
Ramasamy SK, Kusumbe AP, Schiller M, et al. Blood flow controls bone vascular function and osteogenesis[J]. Nat Commun, 2016, 7:13601.
[31]
Liu Y, Chen P, Hu B, et al. Excessive mechanical loading promotes osteoarthritis development by upregulating Rcn2[J]. Biochim Biophys Acta Mol Basis Dis, 2024, 1870(6):167251.
[32]
Sun L, Wang Y, Kan T, et al. Elevated expression of Piezo1 activates the cGAS-STING pathway in chondrocytes by releasing mitochondrial DNA[J]. Osteoarthritis Cartilage, 2025, 33(5):601-615.
[33]
Kageyama A, Matsui H, Ohta M, et al. Palmitic acid induces osteoblastic differentiation in vascular smooth muscle cells through ACSL3 and NF-κB, novel targets of eicosapentaenoic acid[J]. PLoS One, 2013, 8(6):e68197.
[34]
Chen D, Li Y, Zhou Z, et al. HIF-1α inhibits Wnt signaling pathway by activating Sost expression in osteoblasts[J]. PLoS One, 2013, 8(6):e65940.
[35]
Liu L, Yuan W, Wang J. Mechanisms for osteogenic differentiation of human mesenchymal stem cells induced by fluid shear stress[J]. Biomech Model Mechanobiol, 2010, 9(6):659-670.
[36]
Andreev D, Liu M, Weidner D, et al. Osteocyte necrosis triggers osteoclast-mediated bone loss through macrophage-inducible C-type lectin[J]. J Clin Invest, 2020, 130(9):4811-4830.
[37]
Millerand M, Berenbaum F, Jacques C. Danger signals and inflammaging in osteoarthritis[J]. Clin Exp Rheumatol, 2019, 37 Suppl 120(5):48-56.
[38]
Sohn R, Assar T, Kaufhold I, et al. Osteoarthritis patients exhibit an autonomic dysfunction with indirect sympathetic dominance[J]. J Transl Med, 2024, 22(1):467.
[39]
Spindler JS, Henning RJ. The critical role of inflammation in atherosclerotic coronary artery heart disease[J]. Curr Probl Cardiol, 2026, 51(7):103261.
[40]
Hashimoto K, Akagi M. The role of oxidation of low-density lipids in pathogenesis of osteoarthritis: A narrative review[J]. J Int Med Res, 2020, 48(6):300060520931609.
[41]
Dessalles CA, Leclech C, Castagnino A, et al. Integration of substrate- and flow-derived stresses in endothelial cell mechanobiology[J]. Commun Biol, 2021, 4(1):764.
[42]
Tootsi K, Märtson A, Zilmer M, et al. Increased arterial stiffness in patients with end-stage osteoarthritis: A case-control study[J]. BMC Musculoskelet Disord, 2016, 17:335.
[43]
Liu S, Deng Z, Chen K, et al. Cartilage tissue engineering: From proinflammatory and anti-inflammatory cytokines to osteoarthritis treatments (Review)[J]. Mol Med Rep, 2022, 25(3):12615.
[44]
Van Der Kraan PM. Differential role of transforming growth factor-beta in an osteoarthritic or a healthy joint[J]. J Bone Metab, 2018, 25(2):65-72.
[45]
Olansen J, Aaron RK. Similar Pathophysiological mechanisms between osteoarthritis and vascular disease[J]. Front Biosci (Landmark Ed), 2024, 29(9):320.
[46]
Fernandes JC, Martel-Pelletier J, Pelletier JP. The role of cytokines in osteoarthritis pathophysiology[J]. Biorheology, 2002, 39(1-2):237-246.
[47]
Ertürk C, Altay MA, Bilge A, et al. Is there a relationship between serum ox-LDL, oxidative stress, and PON1 in knee osteoarthritis?[J]. Clin Rheumatol, 2017, 36(12):2775-2780.
[48]
Shang L, Wang W, Liu Y, et al. Circulating proteomics and risk of atrial fibrillation: A systematic review of cohort studies[J]. J Cell Mol Med, 2025, 29(15):e70760.
[49]
Yu ZC, Fu R, Li Y, et al. The STING inhibitor C-176 attenuates osteoclast-related osteolytic diseases by inhibiting osteoclast differentiation[J]. Faseb J, 2023, 37(4):e22867.
[50]
Yao C, Veleva T, Scott L, et al. Enhanced cardiomyocyte NLRP3 inflammasome signaling promotes atrial fibrillation[J]. Circulation, 2018, 138(20):2227-2242.
[51]
Cao H, Wang J, Xi L, et al. Dysregulated atrial gene expression of osteoprotegerin/receptor activator of nuclear factor-κB (RANK)/RANK ligand axis in the development and progression of atrial fibrillation[J]. Circ J, 2011, 75(12): 2781-2788.
[52]
Kan S, Duan M, Liu Y, et al. Role of mitochondria in physiology of chondrocytes and diseases of osteoarthritis and rheumatoid arthritis[J]. Cartilage, 2021, 13(2 suppl):1102s-1121s.
[53]
Chang Y, Zou Q. Mitochondrial calcium homeostasis and atrial fibrillation: Mechanisms and therapeutic strategies review[J]. Curr Probl Cardiol, 2025, 50(3):102988.
[54]
Adamo L, Rocha-Resende C, Prabhu SD, et al. Reappraising the role of inflammation in heart failure[J]. Nat Rev Cardiol, 2020, 17(5):269-85.
[55]
Palumbo A, Atzeni F, Murdaca G, et al. The role of alarmins in osteoarthritis pathogenesis: HMGB1, S100B and IL-33[J]. Int J Mol Sci, 2023, 24(15):12143.
[56]
Lu J, Zhao Q, Wang L, et al. MBNL2 promotes aging-related cardiac fibrosis via inhibited SUMOylation of Krüppel-like factor4[J]. iScience, 2024, 27(7):110163.
[57]
Andenæs K, Lunde IG, Mohammadzadeh N, et al. The extracellular matrix proteoglycan fibromodulin is upregulated in clinical and experimental heart failure and affects cardiac remodeling[J]. PLoS One, 2018, 13(7):e0201422.
[58]
Zhao F, Bai Y, Xiang X, et al. The role of fibromodulin in inflammatory responses and diseases associated with inflammation[J]. Front Immunol, 2023, 14:1191787.
[59]
杨剑锋,郝琳,王岩,等.骨关节炎与心血管疾病交互影响的研究进展[J].基础医学与临床202545(2):148-153.
[60]
Shimizu H, Nakagami H, Osako MK, et al. AngiotensinⅡ accelerates osteoporosis by activating osteoclasts[J]. Faseb J, 2008, 22(7):2465-2475.
[61]
Ren J, Kitaura H, Noguchi T, et al. Exogenous angiotensin-(1-7) provides protection against inflammatory bone resorption and osteoclastogenesis by inhibition of TNF-α expression in macrophages[J]. Calcif Tissue Int, 2024, 115(4):432-444.
[62]
Mo C, Ke J, Zhao D, et al. Role of the renin-angiotensin-aldosterone system in bone metabolism[J]. J Bone Miner Metab, 2020, 38(6):772-779.
[63]
Delalio LJ, Sved AF, Stocker SD. Sympathetic nervous system contributions to hypertension: Updates and therapeutic relevance[J]. Can J Cardiol, 2020, 36(5):712-720.
[64]
Lean JM, Jagger CJ, Kirstein B, et al. Hydrogen peroxide is essential for estrogen-deficiency bone loss and osteoclast formation[J]. Endocrinology, 2005, 146(2):728-735.
[65]
Madhur MS, Lob HE, Mccann LA, et al. Interleukin 17 promotes angiotensinⅡ-induced hypertension and vascular dysfunction[J]. Hypertension, 2010, 55(2):500-507.
[66]
Peng R, Dong Y, Zheng M, et al. IL-17 promotes osteoclast-induced bone loss by regulating glutamine-dependent energy metabolism[J]. Cell Death Dis, 2024, 15(2):111.
[67]
Ilić K, Obradović N, Vujasinović-Stupar N. The relationship among hypertension, antihypertensive medications, and osteoporosis: A narrative review[J]. Calcif Tissue Int, 2013, 92(3):217-227.
[68]
Duang S, Zhang M, Liu C, et al. Parathyroid hormone-induced vascular smooth muscle cells calcification by endoplasmic reticulum stress[J]. J Physiol Pharmacol, 2022, 73(5):3.
[69]
Bao Z, Du J, Gao Y, et al. Egg yolk-derived peptide VPF orchestrates OPG/RANKL/RANK-Mediated signaling to suppress osteoclast differentiation and facilitate bone development in zebrafish[J]. ACS Omega, 2026, 11(25):37486-37499.
[70]
Zhang X, Sun Q, Xie X, et al. Epimedin B protects against bone loss and inflammation in diabetic osteoporosis rats by regulating OPG/RANKL pathway[J]. J Orthop Surg Res, 2025, 20(1):403.
[71]
Lee HK, Notario GR, Won SY, et al. Elevated sclerostin levels contribute to reduced bone mineral density in non-ambulatory stroke patients[J]. Bone Rep, 2025, 25:101829.
[72]
Whitehead M, Faleeva M, Oexner R, et al. ECM Modifications driven by age and metabolic stress directly promote vascular smooth muscle cell osteogenic processes[J]. Arterioscler Thromb Vasc Biol, 2025, 45(3):424-442.
[73]
Capulli M, Paone R, Rucci N. Osteoblast and osteocyte: Games without frontiers [J]. Arch Biochem Biophys, 2014, 561:3-12.
[74]
Morrell NW, Bloch DB, Ten Dijke P, et al. Targeting BMP signalling in cardiovascular disease and anaemia[J]. Nat Rev Cardiol, 2016, 13(2):106-120.
[75]
Zhu D, Li X, Macrae VE, et al. Extragonadal effects of follicle-stimulating hormone on osteoporosis and cardiovascular disease in women during menopausal transition[J]. Trends Endocrinol Metab, 2018, 29(8):571-580.
[76]
Neumann E, Junker S, Schett G, et al. Adipokines in bone disease[J]. Nat Rev Rheumatol, 2016, 12(5):296-302.
[77]
Cao H, Li Q, Li M, et al. Osteoprotegerin/RANK/RANKL axis and atrial remodeling in mitral valvular patients with atrial fibrillation [J]. Int J Cardiol, 2013, 166(3):702-708.
[78]
Xi L, Cao H, Chen Y. OPG/RANK/RANKL axis in atrial fibrillation[J]. Cardiology, 2013, 125(3):174-175.
[79]
Pani P, Swalsingh G, Sadayappan S, et al. Emerging roles of micropeptides in calcium cycling dysregulation and atrial fibrillation: A review[J]. Int J Biol Macromol, 2026, 370:152923.
[80]
Guan Z, Yuan W, Jia J, et al. Bone mass loss in chronic heart failure is associated with sympathetic nerve activation[J]. Bone, 2023, 166:116596.
[81]
Xue L, Guan Q, Zhang L. Bone modelling and remodelling in cold environment[J]. Biomolecules, 2025, 15(4).
[82]
Zheng MH, Li FX, Xu F, et al. The interplay between the renin-angiotensin-aldosterone system and parathyroid hormone[J]. Front Endocrinol (Lausanne), 2020, 11:539.
[83]
Ge G, Li J, Wang Q. Heart failure and fracture risk: A meta-analysis[J]. Osteoporos Int, 2019, 30(10):1903-1909.
[84]
Loncar G, Cvetinovic N, Lainscak M, et al. Bone in heart failure[J]. J Cachexia Sarcopenia Muscle, 2020, 11(2):381-393.
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