慢性肾脏病肌-骨交互机制的研究进展

参考文献

[1] Kidney disease: improving global outcomes (KDIGO) CKD work group. KDIGO 2024 clinical practice guideline for the evaluation and management of chronic kidney disease[J]. Kidney Int, 2024, 105(4S): S117-S314. DOI: 10.1016/j.kint.2023.10.018.

[2] Malluche H H, Porter D S, Monier-Faugere M C, et al. Differences in bone quality in low- and high-turnover renal osteodystrophy[J]. J Am Soc Nephrol, 2012, 23(3): 525-532. DOI: 10.1681/ASN.2010121253.

[3] Price S R, Wang X H. Protein-energy wasting in chronic kidney disease: mechanisms responsible for loss of muscle mass and function[J]. Kidney Res Clin Pract, 2025, 44(5): 726-740. DOI: 10.23876/j.krcp.24.214.

[4] Kirk B, Lombardi G, Duque G. Bone and muscle crosstalk in ageing and disease[J]. Nat Rev Endocrinol, 2025, 21(6): 375-390. DOI: 10.1038/s41574-025-01088-x.

[5] Johansen K L, Chertow G M, Ng A V, et al. Physical activity levels in patients on hemodialysis and healthy sedentary controls[J]. Kidney Int, 2000, 57(6): 2564-2570. DOI: 10.1046/j.1523-1755.2000.00116.x.

[6] Kuo C P, Tsai M T, Lee K H, et al. Dose-response effects of physical activity on all-cause mortality and major cardiorenal outcomes in chronic kidney disease[J]. Eur J Prev Cardiol, 2022, 29(3): 452-461. DOI: 10.1093/eurjpc/zwaa162.

[7] Sun Lixin, Sun Yingfei, Huang Zhipei, et al. Improved Hill-type musculotendon models with activation-force-length coupling[J]. Technol Health Care, 2018, 26(6): 909-920. DOI: 10.3233/THC-181267.

[8] Guo Jianqiao, Guo Wei, Ren Gexue. Embodiment of intra-abdominal pressure in a flexible multibody model of the trunk and the spinal unloading effects during static lifting tasks[J]. Biomech Model Mechanobiol, 2021, 20(4): 1599-1626. DOI: 10.1007/s10237-021-01465-1.

[9] Lloyd J E, Roewer-Despres F, Stavness I. Muscle path wrapping on arbitrary surfaces[J]. IEEE Trans Biomed Eng, 2021, 68(2): 628-638. DOI: 10.1109/TBME.2020.3009922.

[10] Meyers V E, Zayzafoon M, Gonda S R, et al. Modeled microgravity disrupts collagen I/integrin signaling during osteoblastic differentiation of human mesenchymal stem cells[J]. J Cell Biochem, 2004, 93(4): 697-707. DOI: 10.1002/jcb.20229.

[11] Sun Weijia, Chi Shaopeng, Li Yuheng, et al. The mechanosensitive Piezo1 channel is required for bone formation[J]. Elife, 2019, 8: e47454. DOI: 10.7554/eLife.47454.

[12] Geng Jie, Liu Wenhao, Zhou Heng, et al. A plug-and-latch mechanism for gating the mechanosensitive Piezo channel[J]. Neuron, 2020, 106(3): 438-451. DOI: 10.1016/j.neuron.2020.02.010.

[13] Malone A M, Anderson C T, Tummala P, et al. Primary cilia mediate mechanosensing in bone cells by a calcium-independent mechanism[J]. Proc Natl Acad Sci U S A, 2007, 104(33): 13325-13330. DOI: 10.1073/pnas.0700636104.

[14] Xiao Zhousheng, Zhang Shiqin, Mahlios J, et al. Cilia-like structures and polycystin-1 in osteoblasts/osteocytes and associated abnormalities in skeletogenesis and Runx2 expression[J]. J Biol Chem, 2006, 281(41): 30884-30895. DOI: 10.1074/jbc.M604772200.

[15] Loiselle A E, Jiang J X, Donahue H J. Gap junction and hemichannel functions in osteocytes[J]. Bone, 2013, 54(2): 205-212. DOI: 10.1016/j.bone.2012.08.132.

[16] Elosegui-Artola A, Andreu I, Beedle A E M, et al. Force triggers YAP nuclear entry by regulating transport across nuclear pores[J]. Cell, 2017, 171(6): 1397-1410.e14. DOI: 10.1016/j.cell.2017.10.008.

[17] Kegelman C D, Mason D E, Dawahare J H, et al. Skeletal cell YAP and TAZ combinatorially promote bone development[J]. FASEB J, 2018, 32(5): 2706-2721. DOI: 10.1096/fj.201700872R.

[18] Polkey M I, Praestgaard J, Berwick A, et al. Activin type II receptor blockade for treatment of muscle depletion in chronic obstructive pulmonary disease. A randomized trial[J]. Am J Respir Crit Care Med, 2019, 199(3): 313-320. DOI: 10.1164/rccm.201802-0286OC.

[19] Bataille S, Chauveau P, Fouque D, et al. Myostatin and muscle atrophy during chronic kidney disease[J]. Nephrol Dial Transplant, 2021, 36(11): 1986-1993. DOI: 10.1093/ndt/gfaa129.

[20] Kellum E, Starr H, Arounleut P, et al. Myostatin (GDF-8) deficiency increases fracture callus size, Sox-5 expression, and callus bone volume[J]. Bone, 2009, 44(1): 17-23. DOI: 10.1016/j.bone.2008.08.126.

[21] Dankbar B, Fennen M, Brunert D, et al. Myostatin is a direct regulator of osteoclast differentiation and its inhibition reduces inflammatory joint destruction in mice[J]. Nat Med, 2015, 21(9): 1085-1090. DOI: 10.1038/nm.3917.

[22] Yasar E, Tek N A, Tekbudak M Y, et al. The relationship between myostatin, inflammatory markers, and sarcopenia in patients with chronic kidney disease[J]. J Ren Nutr, 2022, 32(6): 677-684. DOI: 10.1053/j.jrn.2022.01.011.

[23] Rooks D, Praestgaard J, Hariry S, et al. Treatment of sarcopenia with bimagrumab: results from a phase II, randomized, controlled, proof-of-concept study[J]. J Am Geriatr Soc, 2017, 65(9): 1988-1995. DOI: 10.1111/jgs.14927.

[24] Becker C, Lord S R, Studenski S A, et al. Myostatin antibody (LY2495655) in older weak fallers: a proof-of-concept, randomised, phase 2 trial[J]. Lancet Diabetes Endocrinol, 2015, 3(12): 948-957. DOI: 10.1016/S2213-8587(15)00298-3.

[25] Woodhouse L, Gandhi R, Warden S J, et al. A phase 2 randomized study investigating the efficacy and safety of myostatin antibody LY2495655 versus placebo in patients undergoing elective total hip arthroplasty[J]. J Frailty Aging, 2016, 5(1): 62-70. DOI: 10.14283/jfa.2016.81.

[26] Munoz-Canoves P, Scheele C, Pedersen B K, et al. Interleukin-6 myokine signaling in skeletal muscle: a double-edged sword?[J]. FEBS J, 2013, 280(17): 4131-4148. DOI: 10.1111/febs.12338.

[27] Liu Hongrui, Feng Wei, Yimin, et al. Histological evidence of increased osteoclast cell number and asymmetric bone resorption activity in the tibiae of interleukin-6-deficient mice[J]. J Histochem Cytochem, 2014, 62(8): 556-564. DOI: 10.1369/0022155414537830.

[28] Quinn L S, Anderson B G, Strait-Bodey L, et al. Oversecretion of interleukin-15 from skeletal muscle reduces adiposity[J]. Am J Physiol Endocrinol Metab, 2009, 296(1): E191-E202. DOI: 10.1152/ajpendo.90506.2008.

[29] Djaafar S, Pierroz D D, Chicheportiche R, et al. Inhibition of T cell-dependent and RANKL-dependent osteoclastogenic processes associated with high levels of bone mass in interleukin-15 receptor-deficient mice[J]. Arthritis Rheum, 2010, 62(11): 3300-3310. DOI: 10.1002/art.27645.

[30] Takeda H, Kikuchi T, Soboku K, et al. Effect of IL-15 and natural killer cells on osteoclasts and osteoblasts in a mouse coculture[J]. Inflammation, 2014, 37(3): 657-669. DOI: 10.1007/s10753-013-9782-0.

[31] Wang X H, Mitch W E, Price S R. Pathophysiological mechanisms leading to muscle loss in chronic kidney disease[J]. Nat Rev Nephrol, 2022, 18(3): 138-152. DOI: 10.1038/s41581-021-00498-0.

[32] Bostrom P, Wu Jun, Jedrychowski M P, et al. A PGC1-alpha-dependent myokine that drives brown-fat-like development of white fat and thermogenesis[J]. Nature, 2012, 481(7382): 463-468. DOI: 10.1038/nature10777.

[33] Sadeghi Shad J, Akbari R, Qujeq D, et al. Measurement of serum irisin in the different stages of chronic kidney disease[J]. Caspian J Intern Med, 2019, 10(3): 314-319. DOI: 10.22088/cjim.10.3.314.

[34] Reza M M, Subramaniyam N, Sim C M, et al. Irisin is a pro-myogenic factor that induces skeletal muscle hypertrophy and rescues denervation-induced atrophy[J]. Nat Commun, 2017, 8(1): 1104. DOI: 10.1038/s41467-017-01131-0.

[35] Colaianni G, Cuscito C, Mongelli T, et al. The myokine irisin increases cortical bone mass[J]. Proc Natl Acad Sci U S A, 2015, 112(39): 12157-12162. DOI: 10.1073/pnas.1516622112.

[36] Anastasilakis A D, Polyzos S A, Makras P, et al. Circulating irisin is associated with osteoporotic fractures in postmenopausal women with low bone mass but is not affected by either teriparatide or denosumab treatment for 3 months[J]. Osteoporos Int, 2014, 25(5): 1633-1642. DOI: 10.1007/s00198-014-2673-x.

[37] Wu Meng, Li Huilian, Sun Xiaoting, et al. Aerobic exercise prevents renal osteodystrophy via irisin-activated osteoblasts[J]. JCI Insight, 2025, 10(5): e184468. DOI: 10.1172/jci.insight.184468.

[38] Bozic M, Betriu A, Bermudez-Lopez M, et al. Association of FGF-2 concentrations with atheroma progression in chronic kidney disease patients[J]. Clin J Am Soc Nephrol, 2018, 13(4): 577-584. DOI: 10.2215/CJN.07980717.

[39] Adhikary S, Choudhary D, Tripathi A K, et al. FGF-2 targets sclerostin in bone and myostatin in skeletal muscle to mitigate the deleterious effects of glucocorticoid on musculoskeletal degradation[J]. Life Sci, 2019, 229: 261-276. DOI: 10.1016/j.lfs.2019.05.022.

[40] Shimada T, Hasegawa H, Yamazaki Y, et al. FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis[J]. J Bone Miner Res, 2004, 19(3): 429-435. DOI: 10.1359/JBMR.0301264.

[41] Beben T, Ix J H, Shlipak M G, et al. Fibroblast growth factor-23 and frailty in elderly community-dwelling individuals: the cardiovascular health study[J]. J Am Geriatr Soc, 2016, 64(2): 270-276. DOI: 10.1111/jgs.13951.

[42] Kido S, Hashimoto Y, Segawa H, et al. Muscle atrophy in patients wirh CKD results from FGF23/klotho-mediated supression of insulin/IGF-I signaling[J]. Kidney Res Clin Pract, 2012, 31(2): A44. DOI: 10.1016/j.krcp.2012.04.435.

[43] Sato C, Iso Y, Mizukami T, et al. Fibroblast growth factor-23 induces cellular senescence in human mesenchymal stem cells from skeletal muscle[J]. Biochem Biophys Res Commun, 2016, 470(3): 657-662. DOI: 10.1016/j.bbrc.2016.01.086.

[44] Elsurer Afsar R, Afsar B, Ikizler T A. Fibroblast growth factor 23 and muscle wasting: a metabolic point of view[J]. Kidney Int Rep, 2023, 8(7): 1301-1314. DOI: 10.1016/j.ekir.2023.04.027.

[45] Hu M C, Kuro-o M, Moe O W. Klotho and chronic kidney disease[J]. Contrib Nephrol, 2013, 180: 47-63. DOI: 10.1159/000346778.

[46] Alpdemir M, Fidancı V, Alpdemir M F, et al. Serum undercarboxylated osteocalcin levels are related to bone disease in hemodialysis and peritoneal dialysis patients[J]. Eur Res J, 2021, 7(3): 225-234. DOI: 10.18621/EURJ.734216.

[47] Mera P, Laue K, Ferron M, et al. Osteocalcin signaling in myofibers is necessary and sufficient for optimum adaptation to exercise[J]. Cell Metab, 2016, 23(6): 1078-1092. DOI: 10.1016/j.cmet.2016.05.004.

[48] Mera P, Laue K, Wei Jianwen, et al. Osteocalcin is necessary and sufficient to maintain muscle mass in older mice[J]. Mol Metab, 2016, 5(10): 1042-1047. DOI: 10.1016/j.molmet.2016.07.002.

[49] Moriishi T, Ozasa R, Ishimoto T, et al. Osteocalcin is necessary for the alignment of apatite crystallites, but not glucose metabolism, testosterone synthesis, or muscle mass[J]. PLoS Genet, 2020, 16(5): e1008586. DOI: 10.1371/journal.pgen.1008586.

[50] Diegel C R, Hann S, Ayturk U M, et al. An osteocalcin-deficient mouse strain without endocrine abnormalities[J]. PLoS Genet, 2020, 16(5): e1008361. DOI: 10.1371/journal.pgen.1008361.

[51] Dufresne S S, Boulanger-Piette A, Bosse S, et al. Genetic deletion of muscle RANK or selective inhibition of RANKL is not as effective as full-length OPG-fc in mitigating muscular dystrophy[J]. Acta Neuropathol Commun, 2018, 6(1): 31. DOI: 10.1186/s40478-018-0533-1.

[52] Park S, Jia T, Qureshi A R, et al. Determinants and survival implications of low bone mineral density in end-stage renal disease patients[J]. J Nephrol, 2013, 26(3): 485-494. DOI: 10.5301/jn.5000185.

[53] Chan C K F, Gulati G S, Sinha R, et al. Identification of the human skeletal stem cell[J]. Cell, 2018, 175(1): 43-56. DOI: 10.1016/j.cell.2018.07.029.

[54] Zhou B O, Yue R, Murphy M M, et al. Leptin-receptor-expressing mesenchymal stromal cells represent the main source of bone formed by adult bone marrow[J]. Cell Stem Cell, 2014, 15(2): 154-168. DOI: 10.1016/j.stem.2014.06.008.

[55] Matsushita Y, Nagata M, Kozloff K M, et al. A Wnt-mediated transformation of the bone marrow stromal cell identity orchestrates skeletal regeneration[J]. Nat Commun, 2020, 11(1): 332. DOI: 10.1038/s41467-019-14029-w.

[56] Zhao H, Feng J, Ho T, et al. The suture provides a niche for mesenchymal stem cells of craniofacial bones[J]. Nat Cell Biol, 2015, 17(4): 386-396. DOI: 10.1038/ncb3139.

[57] Duchamp De Lageneste O, Julien A, Abou-Khalil R, et al. Periosteum contains skeletal stem cells with high bone regenerative potential controlled by Periostin[J]. Nat Commun, 2018, 9(1): 773. DOI: 10.1038/s41467-018-03124-z.

[58] Debnath S, Yallowitz A R, Mccormick J, et al. Discovery of a periosteal stem cell mediating intramembranous bone formation[J]. Nature, 2018, 562(7725): 133-139. DOI: 10.1038/s41586-018-0554-8.

[59] Wolf M, White K E. Coupling fibroblast growth factor 23 production and cleavage: iron deficiency, rickets, and kidney disease[J]. Curr Opin Nephrol Hypertens, 2014, 23(4): 411-419. DOI: 10.1097/01.mnh.0000447020.74593.6f.

[60] Sabbagh Y, Graciolli F G, O'Brien S, et al. Repression of osteocyte Wnt/beta-catenin signaling is an early event in the progression of renal osteodystrophy[J]. J Bone Miner Res, 2012, 27(8): 1757-1772. DOI: 10.1002/jbmr.1630.

[61] Doyon A, Fischer D C, Bayazit A K, et al. Markers of bone metabolism are affected by renal function and growth hormone therapy in children with chronic kidney disease[J]. PLoS One, 2015, 10(2): e0113482. DOI: 10.1371/journal.pone.0113482.

[62] Abou-Khalil R, Yang F, Lieu S, et al. Role of muscle stem cells during skeletal regeneration[J]. Stem Cells, 2015, 33(5): 1501-1511. DOI: 10.1002/stem.1945.

[63] Julien A, Kanagalingam A, Martinez-Sarra E, et al. Direct contribution of skeletal muscle mesenchymal progenitors to bone repair[J]. Nat Commun, 2021, 12(1): 2860. DOI: 10.1038/s41467-021-22842-5.

[64] Avin K G, Chen N X, Organ J M, et al. Skeletal muscle regeneration and oxidative stress are altered in chronic kidney disease[J]. PLoS One, 2016, 11(8): e0159411. DOI: 10.1371/journal.pone.0159411.

[65] Chuang S Y, Chang H Y, Lee M S, et al. Skeletal muscle mass and risk of death in an elderly population[J]. Nutr Metab Cardiovasc Dis, 2014, 24(7): 784-791. DOI: 10.1016/j.numecd.2013.11.010.

[66] Sitara D, Razzaque M S, St-Arnaud R, et al. Genetic ablation of vitamin D activation pathway reverses biochemical and skeletal anomalies in Fgf-23-null animals[J]. Am J Pathol, 2006, 169(6): 2161-2170. DOI: 10.2353/ajpath.2006.060329.