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. Author manuscript; available in PMC: 2013 May 1.
Published in final edited form as: Semin Nephrol. 2012 May;32(3):295–303. doi: 10.1016/j.semnephrol.2012.04.009

Figure 1.

Figure 1

TGF-β targets in mitochondria. TGF-β signaling may act in a direct or indirect manner to control mitochondrial metabolism in different cell types. ⍊ and ↓ indicate inhibition/downregulation by TGF-β pathway. Oxidative phosphorylation system (I-V), membrane potential (ΔΨ), reactive oxygen species (ROS), endoplasmic reticulum (ER). Inhibition of the oxidative phosphorylation system may arise from a direct inhibition of complex IV and/or from increased ROS production due to downregulation of scavenging proteins (MnSOD, Mpv17l). Decrease in membrane potential is associated with cytochrome c release in the cytoplasm with consequent activation of the apoptotic signaling. Apoptosis can be triggered by release of HtrA2 as a consequence of Mpv17l downregulation. Uncoupling of mitochondria from ER calcium release may impair the intracellular calcium sensing responses.