Swimming exercise prevents fibrogenesis in chronic kidney disease by inhibiting the myofibroblast transdifferentiation

Chiung Chi Peng, Kuan Chou Chen, Chiu Lan Hsieh, Robert Y. Peng

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

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.

Original languageEnglish
Article numbere37388
JournalPLoS ONE
Volume7
Issue number6
DOIs
Publication statusPublished - 2012 Jun 27

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Myofibroblasts
kidney diseases
Chronic Renal Insufficiency
exercise
Exercise
Doxorubicin
doxorubicin
Glomerular Mesangium
Matrix Metalloproteinases
Rats
glomerulonephritis
gelatinase A
gelatinase B
Mesangial Cells
Collagen
disease models
Chemical activation
Blood Urea Nitrogen
hyperlipidemia
renal function

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)
  • General

Cite this

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abstract = "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.",
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Swimming exercise prevents fibrogenesis in chronic kidney disease by inhibiting the myofibroblast transdifferentiation. / Peng, Chiung Chi; Chen, Kuan Chou; Hsieh, Chiu Lan; Peng, Robert Y.

In: PLoS ONE, Vol. 7, No. 6, e37388, 27.06.2012.

Research output: Contribution to journalArticle

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