Mitochondrial proteases modulate mitochondrial stress signalling and cellular homeostasis in health and disease

dc.contributor.authorMoisoi, Nicoleta
dc.date.acceptance2024
dc.date.accessioned2024-07-09T14:55:10Z
dc.date.available2024-07-09T14:55:10Z
dc.date.issued2024-06-19
dc.descriptionopen access article
dc.description.abstractMaintenance of mitochondrial homeostasis requires a plethora of coordinated quality control and adaptations’ mechanisms in which mitochondrial proteases play a key role. Their activation or loss of function reverberate beyond local mitochondrial biochemical and metabolic remodelling into coordinated cellular pathways and stress responses that feedback onto the mitochondrial functionality and adaptability. Mitochondrial proteolysis modulates molecular and organellar quality control, metabolic adaptations, lipid homeostasis and regulates transcriptional stress responses. Defective mitochondrial proteolysis results in disease conditions most notably, mitochondrial diseases, neurodegeneration and cancer. Here, it will be discussed how mitochondrial proteases and mitochondria stress signalling impact cellular homeostasis and determine the cellular decision to survive or die, how these processes may impact disease etiopathology, and how modulation of proteolysis may offer novel therapeutic strategies.
dc.funderNo external funder
dc.identifier.citationMoisoi, N. (2024) Mitochondrial proteases modulate mitochondrial stress signalling and cellular homeostasis in health and disease. Biochimie,
dc.identifier.doihttps://doi.org/10.1016/j.biochi.2024.06.005
dc.identifier.urihttps://hdl.handle.net/2086/23993
dc.peerreviewedYes
dc.publisherElsevier
dc.researchinstituteLeicester Institute for Pharmaceutical Innovation - From Molecules to Practice (LIPI)
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.titleMitochondrial proteases modulate mitochondrial stress signalling and cellular homeostasis in health and disease
dc.typeArticle

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