[1] Sato E, Mori T, Mishima E, et al. Metabolic alterations by indoxyl sulfate in skeletal muscle induce uremic sarcopenia in chronic kidney disease [J]. Sci Rep, 2016, 6:36618.[2] Enoki Y, Watanabe H, Arake R, et al. Indoxyl sulfate potentiates skeletal muscle atrophy by inducing the oxidative stress-mediated expression of myostatin and atrogin-1 [J]. Sci Rep, 2016, 6:32084.[3] Enoki Y, Watanabe H, Arake R, et al. Potential therapeutic interventions for chronic kidney disease-associated sarcopenia via indoxyl sulfate-induced mitochondrial dysfunction [J]. J Cachexia Sarcopenia Muscle, 2017, 8(5): 735-747.[4] Vidoni ML, Pettee Gabriel K, Luo ST, et al. Relationship between Homocysteine and Muscle Strength Decline: The Baltimore Longitudinal Study of Aging [J]. J Gerontol A Biol Sci Med Sci, 2018, 73(4): 546-551.[5] Majumder A, Singh M, Behera J, et al. Hydrogen sulfide alleviates hyperhomocysteinemia-mediated skeletal muscle atrophy via mitigation of oxidative and endoplasmic reticulum stress injury [J]. Am J Physiol Cell Physiol, 2018, 315(5): C609-C622.[6] Veeranki S, Lominadze D, Tyagi SC. Hyperhomocysteinemia inhibits satellite cell regenerative capacity through p38 alpha/beta MAPK signaling [J]. Am J Physiol Heart Circ Physiol, 2015, 309(2): H325-334.[7] Kraut J A, Madias NE. Metabolic acidosis: pathophysiology, diagnosis and management [J]. Nat Rev Nephrol, 2010, 6(5): 274-285.[8] May R C, Kelly RA, Mitch WE. Metabolic acidosis stimulates protein degradation in rat muscle by a glucocorticoid-dependent mechanism [J]. J Clin Invest, 1986, 77(2): 614-621.[9] Sato AY, Richardson D, Cregor M, et al. Glucocorticoids Induce Bone and Muscle Atrophy by Tissue-Specific Mechanisms Upstream of E3 Ubiquitin Ligases [J]. Endocrinology, 2017, 158(3): 664-677.[10] Mutsvangwa T, Gilmore J, Squires JE, et al. Chronic metabolic acidosis increases mRNA levels for components of the ubiquitin-mediated proteolytic pathway in skeletal muscle of dairy cows [J]. J Nutr, 2004, 134(3): 558-561.[11] Pickering WP, Baker FE, Brown J, et al. Glucocorticoid antagonist RU38486 fails to block acid-induced muscle wasting in vivo or in vitro [J]. Nephrol Dial Transplant, 2003, 18(8): 1475-1484.[12] Evans K, Nasim Z, Brown J, et al. Inhibition of SNAT2 by metabolic acidosis enhances proteolysis in skeletal muscle [J]. J Am Soc Nephrol, 2008, 19(11): 2119-2129.[13] Romanova Y, Laikov A, Markelova M, et al. Proteomic Analysis of Human Serum from Patients with Chronic Kidney Disease [J]. Biomolecules, 2020, 10(2): [14] Verzola D, Bonanni A, Sofia A, et al. Toll-like receptor 4 signalling mediates inflammation in skeletal muscle of patients with chronic kidney disease [J]. J Cachexia Sarcopenia Muscle, 2017, 8(1): 131-144.[15] Silva KA, Dong J, Dong Y, et al. Inhibition of Stat3 activation suppresses caspase-3 and the ubiquitin-proteasome system, leading to preservation of muscle mass in cancer cachexia [J]. J Biol Chem, 2015, 290(17): 11177-11187.[16] Ma JF, Sanchez BJ, Hall DT, et al. STAT3 promotes IFNgamma/TNFalpha-induced muscle wasting in an NF-kappaB-dependent and IL-6-independent manner [J]. EMBO Mol Med, 2017, 9(5): 622-637.[17] Zhang G, Liu Z, Ding H, et al. Toll-like receptor 4 mediates Lewis lung carcinoma-induced muscle wasting via coordinate activation of protein degradation pathways [J]. Sci Rep, 2017, 7(1): 2273.[18] Schulz A, Jankowski J, Zidek W, et al. Absolute quantification of endogenous angiotensin II levels in human plasma using ESI-LC-MS/MS [J]. Clin Proteomics, 2014, 11(1): 37.[19] Du Bois P, Pablo Tortola C, Lodka D, et al. Angiotensin II Induces Skeletal Muscle Atrophy by Activating TFEB-Mediated MuRF1 Expression [J]. Circ Res, 2015, 117(5): 424-436.[20] Shen C, Zhou J, Wang X, et al. Angiotensin-II-induced Muscle Wasting is Mediated by 25-Hydroxycholesterol via GSK3beta Signaling Pathway [J]. EBioMedicine, 2017, 16(238-250.[21] Liu Y, Bi X, Zhang Y, et al. Mitochondrial dysfunction/NLRP3 inflammasome axis contributes to angiotensin II-induced skeletal muscle wasting via PPAR-gamma [J]. Lab Invest, 2020, 100(5): 712-726.[22] Ros S, Carrero JJ. Endocrine alterations and cardiovascular risk in CKD: is there a link? [J]. Nefrologia, 2013, 33(2): 181-187.[23] Cigarran S, Pousa M, Castro MJ, et al. Endogenous testosterone, muscle strength, and fat-free mass in men with chronic kidney disease [J]. J Ren Nutr, 2013, 23(5): e89-95.[24] Chiang J M, Kaysen GA, Segal M, et al. Low testosterone is associated with frailty, muscle wasting and physical dysfunction among men receiving hemodialysis: a longitudinal analysis [J]. Nephrol Dial Transplant, 2019, 34(5): 802-810.[25] Dalbo VJ, Roberts MD, Mobley CB, et al. Testosterone and trenbolone enanthate increase mature myostatin protein expression despite increasing skeletal muscle hypertrophy and satellite cell number in rodent muscle [J]. Andrologia, 2017, 49(3): [26] Ghanim H, Dhindsa S, Batra M, et al. Effect of Testosterone on FGF2, MRF4, and Myostatin in Hypogonadotropic Hypogonadism: Relevance to Muscle Growth [J]. J Clin Endocrinol Metab, 2019, 104(6): 2094-2102.[27] Pronsato L, Milanesi L, Vasconsuelo A, et al. Testosterone modulates FoxO3a and p53-related genes to protect C2C12 skeletal muscle cells against apoptosis [J]. Steroids, 2017, 124(35-45.[28] Schaefer F, Veldhuis JD, Stanhope R, et al. Alterations in growth hormone secretion and clearance in peripubertal boys with chronic renal failure and after renal transplantation. Cooperative Study Group of Pubertal development in Chronic Renal Failure [J]. J Clin Endocrinol Metab, 1994, 78(6): 1298-1306.[29] Krieg RJ, Jr., Veldhuis JD, Thornhill BA, et al. Growth hormone (GH) secretion, GH-dependent gene expression, and sexually dimorphic body growth in young rats with chronic renal failure [J]. Endocrine, 2008, 33(3): 323-330.[30] Janjua HS, Mahan JD. Growth in chronic kidney disease [J]. Adv Chronic Kidney Dis, 2011, 18(5): 324-331.[31] Greenstein J, Guest S, Tan J C, et al. Circulating growth hormone binding protein levels and mononuclear cell growth hormone receptor expression in uremia [J]. J Ren Nutr, 2006, 16(2): 141-149.[32] Sun DF, Zheng Z, Tummala P, et al. Chronic uremia attenuates growth hormone-induced signal transduction in skeletal muscle [J]. J Am Soc Nephrol, 2004, 15(10): 2630-2636.[33] Mak RH, Cheung WW, Roberts CT, Jr. The growth hormone-insulin-like growth factor-I axis in chronic kidney disease [J]. Growth Horm IGF Res, 2008, 18(1): 17-25.[34] Han DS, Chen YM, Lin SY, et al. Serum myostatin levels and grip strength in normal subjects and patients on maintenance haemodialysis [J]. Clin Endocrinol (Oxf), 2011, 75(6): 857-863.[35] Lun H, Yang W, Zhao S, et al. Altered gut microbiota and microbial biomarkers associated with chronic kidney disease [J]. Microbiologyopen, 2019, 8(4): e00678.[36] Li F, Wang M, Wang J, et al. Alterations to the Gut Microbiota and Their Correlation With Inflammatory Factors in Chronic Kidney Disease [J]. Front Cell Infect Microbiol, 2019, 9(206.[37] Kikuchi M, Ueno M, Itoh Y, et al. Uremic Toxin-Producing Gut Microbiota in Rats with Chronic Kidney Disease [J]. Nephron, 2017, 135(1): 51-60.[38] Liu Y, Li J, Yu J, et al. Disorder of gut amino acids metabolism during CKD progression is related with gut microbiota dysbiosis and metagenome change [J]. J Pharm Biomed Anal, 2018, 149(425-435.[39] de Sire R, Rizzatti G, Ingravalle F, et al. Skeletal muscle-gut axis: emerging mechanisms of sarcopenia for intestinal and extra intestinal diseases [J]. Minerva Gastroenterol Dietol, 2018, 64(4): 351-362.[40] Lahiri S, Kim H, Garcia-Perez I, et al. The gut microbiota influences skeletal muscle mass and function in mice [J]. Sci Transl Med, 2019, 11(502): [41] Nay K, Jollet M, Goustard B, et al. Gut bacteria are critical for optimal muscle function: a potential link with glucose homeostasis [J]. Am J Physiol Endocrinol Metab, 2019, 317(1): E158-E171.[42] Hu L, Klein J D, Hassounah F, et al. Low-frequency electrical stimulation attenuates muscle atrophy in CKD--a potential treatment strategy [J]. J Am Soc Nephrol, 2015, 26(3): 626-635.[43] Moinuddin I, Leehey DJ. A comparison of aerobic exercise and resistance training in patients with and without chronic kidney disease [J]. Adv Chronic Kidney Dis, 2008, 15(1): 83-96.dv Chronic Kidney Dis, 2008, 15(1): 83-96. |