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This study aimed to investigate whether exercise training could attenuate diabetic renal injury via regulating endogenous hydrogen sulfide (H\n                    <jats:sub>2<\/jats:sub>\n                    S) production. First, C57BL\/6 mice were allocated into the control, diabetes, exercise, and diabetes\u00a0+\u00a0exercise groups. Diabetes was induced by intraperitoneal injection of streptozotocin (STZ). Treadmill exercise continued for four weeks. Second, mice was allocated into the control, diabetes, H\n                    <jats:sub>2<\/jats:sub>\n                    S and diabetes\u00a0+\u00a0H\n                    <jats:sub>2<\/jats:sub>\n                    S groups. H\n                    <jats:sub>2<\/jats:sub>\n                    S donor sodium hydrosulfide (NaHS) was intraperitoneally injected once daily for four weeks. STZ\u2010induced diabetic mice exhibited glomerular hypertrophy, tissue fibrosis and increased urine albumin levels, urine protein\u2010 and albumin\u2010to\u2010creatinine ratios, which were relieved by exercise training. Diabetic renal injury was associated with apoptotic cell death, as evidenced by the enhanced caspase\u20103 activity, the increased TdT\u2010mediated dUTP nick\u2010end labeling \u2010positive cells and the reduced expression of anti\u2010apoptotic proteins, all of which were attenuated by exercise training. Exercise training enhanced renal sirtuin 1 (SIRT1) expression in diabetic mice, accompanied by an inhibition of the p53\u2010#ediated pro\u2010apoptotic pathway. Furthermore, exercise training restored the STZ\u2010mediated downregulation of cystathionine\u2010\u03b2\u2010synthase (CBS) and cystathionine\u2010\u03b3\u2010lyase (CSE) and the reduced renal H\n                    <jats:sub>2<\/jats:sub>\n                    S production. NaHS treatment restored SIRT1 expression, inhibited the p53\u2010mediated pro\u2010apoptotic pathway and attenuated diabetes\u2010associated apoptosis and renal injury. In high glucose\u2010treated MPC5 podocytes, NaHS treatment inhibited the p53\u2010mediated pro\u2010apoptotic pathway and podocyte apoptosis in a SIRT1\u2010dependent manner. Collectively, exercise training upregulated CBS\/CSE expression and enhanced the endogenous H\n                    <jats:sub>2<\/jats:sub>\n                    S production in renal tissues, thereby contributing to the modulation of the SIRT1\/p53 apoptosis pathway and improvement of diabetic nephropathy.\n                  <\/jats:p>","DOI":"10.1096\/fj.202100219r","type":"journal-article","created":{"date-parts":[[2021,8,16]],"date-time":"2021-08-16T03:06:57Z","timestamp":1629083217000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":43,"title":["Exercise training ameliorates early diabetic kidney injury by regulating the H\n                    <sub>2<\/sub>\n                    S\/SIRT1\/p53 pathway"],"prefix":"10.1096","volume":"35","author":[{"given":"Lu","family":"Yang","sequence":"first","affiliation":[{"name":"School of Kinesiology The Key Laboratory of Exercise and Health Sciences of Ministry of Education Shanghai 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