Commentary Open Access
Volume 4 | Issue 3 | DOI: https://doi.org/10.33696/Signaling.4.096

F-ATP Synthase Inhibitory Factor 1 in Regulation of Mitochondrial Permeability Transition Pore and Metabolic Reprogramming

  • 1Center for Mitochondrial Genetics and Health, Greater Bay Area Institute of Precision Medicine (Guangzhou), Fudan University, Nansha District, Guangzhou 511400, China
  • 2Tongji University Cancer Center, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, Shanghai 200092, China
+ Affiliations - Affiliations

Corresponding Author

Lishu Guo, guolishu@tongji.edu.cn; guolsh15@gmail.com

Received Date: April 28, 2023

Accepted Date: May 26, 2023


Mitochondrial permeability transition pore (PTP) plays an important role in mitochondrial physiology and cell fate. Emerging studies highlight PTP forms from F-ATP synthase, but whether F-ATP synthase inhibitory factor 1 (IF1) regulates the activity of PTP is basically unknown. We have recently demonstrated that IF1 interacts with p53-CyPD complex and promotes opening of the PTP, and IF1 is necessary for the formation of p53-CyPD complex. IF1, a natural inhibitor of F-ATP synthase, acts as a main driver of metabolic switch to a Warburg phenotype. In this Commentary, we intend to discuss that the PTP may act as an alternative mechanism through which IF1 regulates metabolic reprogramming. The PTP participates in physiological Ca2+/ROS homeostasis and cell fate depending on the open state. The PTP-regulatory role of IF1 provides a clue that IF1 participates in metabolic plasticity probably involving modulation of PTP activity.


Mitochondria, F-ATP synthase inhibitory factor 1, Permeability transition, Metabolic reprogramming, Cyclophilin D, ROS, p53, Transcription factors

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