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Mitochondrial fission triggered by hyperglycemia is mediated by ROCK1 activation in podocytes and endothelial cells

Wenjian Wang1, Yin Wang, Jianyin Long

  • 1Department of Medicine, Nephrology, Baylor College of Medicine, Houston, TX 77030, USA.

Cell Metabolism
|February 14, 2012
PubMed

Insights

Rho-associated coiled coil-containing protein kinase 1 (ROCK1) mediates hyperglycemia-induced mitochondrial fission in diabetic nephropathy. ROCK1 promotes fission by phosphorylating dynamin-related protein-1 (Drp1), offering new therapeutic targets.

Area of Science:

  • Mitochondrial biology
  • Diabetic complications
  • Cell signaling

Background:

  • Mitochondrial dysfunction is implicated in diabetic nephropathy.
  • Hyperglycemia's role in mitochondrial dysfunction is not fully understood.
  • ROCK1's role in mitochondrial dynamics is under investigation.

Purpose of the Study:

  • To investigate the role of ROCK1 in hyperglycemia-induced mitochondrial dysfunction.
  • To elucidate the signaling pathways linking hyperglycemia, ROCK1, and mitochondrial dynamics.

Main Methods:

  • Generated diabetic mouse models with ROCK1 deletions.
  • Created podocyte-specific knockin mice expressing constitutively active ROCK1.
  • Analyzed mitochondrial fission and Drp1 recruitment.

Main Results:

  • ROCK1 mediates hyperglycemia-induced mitochondrial fission by promoting Drp1 recruitment.
  • ROCK1 deletion prevented mitochondrial fission in diabetic mice.
  • Constitutively active ROCK1 in podocytes increased mitochondrial fission.
  • ROCK1 phosphorylates Drp1 at serine 600 to trigger fission.

Conclusions:

  • ROCK1 plays a critical role in hyperglycemia-induced mitochondrial fission.
  • ROCK1 acts via Drp1 phosphorylation to regulate mitochondrial dynamics.
  • ROCK1 is a potential therapeutic target for diabetic nephropathy.

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