Swimming Exercise Prevents Fibrogenesis in Chronic Kidney Disease by Inhibiting the Myofibroblast Transdifferentiation
نویسندگان
چکیده
BACKGROUND The renal function of chronic kidney disease (CKD) patients may be improved by a number of rehabilitative mechanisms. Swimming exercise training was supposed to be beneficial to its recovery. METHODOLOGY/PRINCIPAL FINDINGS Doxorubicin-induced CKD (DRCKD) rat model was performed. Swimming training was programmed three days per week, 30 or 60 min per day for a total period of 11 weeks. Serum biochemical and pathological parameters were examined. In DRCKD, hyperlipidemia was observed. Active mesangial cell activation was evidenced by overexpression of PDGFR, P-PDGFR, MMP-2, MMP-9, α-SMA, and CD34 with a huge amount collagen deposition. Apparent myofibroblast transdifferentiation implicating fibrogenesis in the glomerular mesangium, glomerulonephritis and glomeruloscelorosis was observed with highly elevated proteinuria and urinary BUN excretion. The 60-min swimming exercise but not the 30 min equivalent rescued most of the symptoms. To quantify the effectiveness of exercise training, a physical parameter, i.e. "the strenuosity coefficient" or "the myokine releasing coefficient", was estimated to be 7.154 × 10(-3) pg/mL-J. CONCLUSIONS The 60-min swimming exercise may ameliorate DRCKD by inhibiting the transdifferentiation of myofibroblasts in the glomerular mesangium. Moreover, rehabilitative exercise training to rescue CKD is a personalized remedy. Benefits depend on the duration and strength of exercise, and more importantly, on the individual physiological condition.
منابع مشابه
The Effect of Regular Aerobic Exercise with Garlic Extract on Heart Apoptosis Regulatory Factors in Chronic Kidney Disease
Objective: Physical activity and herbal medicine can inhabit apoptosis with two different mechanisms. The aim of this study was to assess the combined effect of regular aerobic exercise with garlic extract on heart apoptosis regulatory factors in aged rats with chronic kidney disease. Materials and Methods: In this experimental research, 42 aged male Wistar rats (48-52 weeks) were selected and...
متن کاملPharmacological GLI2 inhibition prevents myofibroblast cell-cycle progression and reduces kidney fibrosis.
Chronic kidney disease is characterized by interstitial fibrosis and proliferation of scar-secreting myofibroblasts, ultimately leading to end-stage renal disease. The hedgehog (Hh) pathway transcriptional effectors GLI1 and GLI2 are expressed in myofibroblast progenitors; however, the role of these effectors during fibrogenesis is poorly understood. Here, we demonstrated that GLI2, but not GLI...
متن کاملThe Effect of one Course of Swimming Exercise before Induction of Multiple Sclerosis (MS) on Nerve Growth Factor Levels in Rat’s Brain
Background and Aim: Multiple Sclerosis is a chronic inflammatory disease with unknown etiology in the nervous system. However, exercise routinely for these patients is beneficial, but the effect of pretreatment swimming exercise in this disease has not been fixed. Therefore, the aim of these study was to investigate pretreatment effect of swimming exercise on NGF levels in female Lewis rats wit...
متن کاملAdvanced glycation end products cause epithelial-myofibroblast transdifferentiation via the receptor for advanced glycation end products (RAGE).
Tubulointerstitial disease, a prominent phenomenon in diabetic nephropathy, correlates with decline in renal function. The underlying pathogenic link between chronic hyperglycemia and the development of tubulointerstitial injury has not been fully elucidated, but myofibroblast formation represents a key step in the development of tubulointerstitial fibrosis. RAGE, the receptor for advanced glyc...
متن کاملTubuloepithelial - Myofibroblast Transdifferentiation - Possible Pathogenic Mechanism of Interstitial Fibrosis in Balkan Endemic Nephropathy
Balkan endemic nephropathy (BEN) is a chronic tubulointerstitial disease of unknown etiology. The main morphological feature is interstitial fibrosis and tubular atrophy with absence of inflammatory infiltration. The pathogenesis of BEN is also obscure. Since tubular epithelial cells in the early phase of disease express vimentin as mesenchymal marker in addition to cytokeratin, we could specul...
متن کامل