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The Inner Mitochondrial Membrane

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Cyclophilin D: An Integrator of Mitochondrial Function.

Georgios Amanakis¹, Elizabeth Murphy¹

¹Cardiovascular Branch, NHLBI, National Institutes of Health, Bethesda, MD, United States.

Frontiers in Physiology

|July 7, 2020

Summary

Cyclophilin D (CypD) regulates the mitochondrial permeability transition pore (PTP), a key factor in cell death. Recent studies reveal post-translational modifications of CypD, offering new insights into PTP regulation and potential therapeutic strategies.

Keywords:

ATP synthase cyclophilin D cyclosporine A mitochondrial function peptidyl-prolyl cis-trans isomerase permeability transition pore

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Area of Science:

Mitochondrial biology
Cell death mechanisms
Biochemistry

Background:

Cyclophilin D (CypD) is a mitochondrial enzyme regulating the permeability transition pore (PTP).
PTP opening is linked to cell death and implicated in diseases like ischemia/reperfusion injury, neurodegenerative disorders, and muscular dystrophies.
Inhibiting CypD shows protective effects in disease models, highlighting its therapeutic potential.

Purpose of the Study:

To review recent findings on post-translational modifications (PTMs) of Cyclophilin D.
To explore how these PTMs influence the regulation of the mitochondrial permeability transition pore (PTP).
To deepen the understanding of CypD's mechanisms of action.

Main Methods:

Literature review of recent studies on Cyclophilin D.
Analysis of identified post-translational modifications of CypD.
Synthesis of information regarding PTP regulation by modified CypD.

Main Results:

Several post-translational modifications of CypD have been identified.
These modifications can alter the regulatory activity of CypD on the PTP.
Understanding these modifications is crucial for elucidating CypD's role in disease.

Conclusions:

Post-translational modifications represent a critical layer of regulation for Cyclophilin D.
These modifications impact PTP function and cellular fate.
Further research into CypD PTMs may uncover novel therapeutic targets for diseases involving mitochondrial dysfunction.