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Updated: Feb 23, 2026

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

Published on: January 7, 2013

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Mitochondrial cyclophilin D ablation is associated with the activation of Akt/p70S6K pathway in the mouse kidney

Jelena Klawitter1,2, Alexander Pennington3, Jost Klawitter3

  • 1Department of Anesthesiology, University of Colorado Denver, Aurora, Colorado, USA. Jelena.Klawitter@ucdenver.edu.

Scientific Reports
|September 7, 2017
PubMed

Insights

Mitochondrial protein cyclophilin D (CypD) loss shifts kidney metabolism towards glycolysis. This metabolic reprogramming, particularly in females, may enhance kidney resilience against injury.

Area of Science:

  • Mitochondrial Biology
  • Renal Physiology
  • Metabolic Regulation

Background:

  • Cyclophilin D (CypD) is a key component of the mitochondrial permeability transition pore (MPTP).
  • Understanding CypD's role in kidney bioenergetics is crucial for metabolic disease research.

Purpose of the Study:

  • To investigate the impact of CypD ablation on kidney bioenergetics in mice.
  • To identify sex-specific metabolic and transcriptional changes following CypD loss.

Main Methods:

  • Analysis of kidney bioenergetics in CypD-ablated (Ppif-/-) and wild-type mice.
  • Assessment of metabolic pathways, including glycolysis and Krebs cycle activity.
  • Transcriptional analysis of key metabolic regulators and signaling pathways (Akt, AMPK, p70S6K, ERK1/2, JNK, TGFβ1).

Main Results:

  • CypD loss induces a metabolic shift towards glycolysis and Krebs cycle activity in mouse kidneys.
  • Increased glucose consumption and upregulation of glucose metabolism effectors were observed.
  • Sex-specific differences emerged, with Ppif-/- females exhibiting enhanced pro-survival signaling (ERK1/2) and inhibited pro-apoptotic/fibrotic markers (JNK, TGFβ1).
  • Ppif-/- females demonstrated higher lactate concentrations and ATP/ADP ratios compared to males.

Conclusions:

  • Loss of mitochondrial CypD significantly alters kidney bioenergetics, activating glucose metabolism pathways.
  • These adaptations, particularly pronounced in females, suggest a potential protective mechanism against kidney injury.
  • Further research into these metabolic shifts could inform therapeutic strategies for kidney diseases.

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