ArticleFrontiers in genetics2016
Cyclophilin D Is Involved in the Regulation of Autophagy and Affects the Lifespan of P. anserina in Response to Mitochondrial Oxidative Stress.
Article in Frontiers in genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Mitophagy-related regulated cell death: molecular mechanisms and disease implications.Cell death & disease · 2024Review
- What are the 100 most cited fungal genera?Studies in mycology · 2024Article
- The Interplay Between Autophagy and Regulated Necrosis.Antioxidants & redox signaling · 2023Review
- A Network of Pathways Controlling Cellular Homeostasis Affects the Onset of Senescence inJournal of fungi (Basel, Switzerland) · 2021Review
- Impaired FCells · 2021Article
- Review
- Impact of F1Fo-ATP-synthase dimer assembly factors on mitochondrial function and organismic aging.Microbial cell (Graz, Austria) · 2018Article
- AT 101 induces early mitochondrial dysfunction and HMOX1 (heme oxygenase 1) to trigger mitophagic cell death in glioma cells.Autophagy · 2018Article
- Guidelines and recommendations on yeast cell death nomenclature.Microbial cell (Graz, Austria) · 2018Review
- The path from mitochondrial ROS to aging runs through the mitochondrial permeability transition pore.Aging cell · 2017Review
- Microbial cyclophilins: specialized functions in virulence and beyond.World journal of microbiology & biotechnology · 2017Review
- Autophagy compensates impaired energy metabolism in CLPXP-deficient Podospora anserina strains and extends healthspan.Aging cell · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mitochondrial permeability transition pore plays a key role in programmed cell death and the induction of autophagy. Opening of the pore is regulated by the mitochondrial peptidyl prolyl-cis, trans-isomerase cyclophilin D (CYPD). Previously it was shown in the aging model organism Podospora anserina that PaCYPD abundance increases during aging and that PaCypD overexpressors are characterized by accelerated aging. Here, we describe a role of PaCYPD in the regulation of autophagy. We found that the accelerated aging phenotype observed in a strain overexpressing PaCypD is not metacaspase-dependent but is accompanied by an increase of general autophagy and mitophagy, the selective autophagic degradation of mitochondria. It thus is linked to what has been defined as "autophagic cell death" or "type II" programmed cell death. Moreover, we found that the previously demonstrated age-related induction of autophagy in wild-type aging depends on the presence of PaCYPD. Deletion of PaCypD leads to a decrease in autophagy in later stages of age and under paraquat-mediated oxidative stress. Finally, we report that PaCYPD is also required for mitohormesis, the beneficial effect of mild mitochondrial stress. Thus, PaCYPD plays a key role in the context-dependent regulation of pathways leading to pro-survival and pro-death effects of autophagy.
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