Mitophagy-driven metabolic switch reprograms stem cell fate.


Journal

Cellular and molecular life sciences : CMLS
ISSN: 1420-9071
Titre abrégé: Cell Mol Life Sci
Pays: Switzerland
ID NLM: 9705402

Informations de publication

Date de publication:
Jan 2019
Historique:
received: 27 07 2018
accepted: 19 09 2018
revised: 12 09 2018
pubmed: 30 9 2018
medline: 23 1 2019
entrez: 30 9 2018
Statut: ppublish

Résumé

"Cellular reprogramming" facilitates the generation of desired cellular phenotype through the cell fate transition by affecting the mitochondrial dynamics and metabolic reshuffle in the embryonic and somatic stem cells. Interestingly, both the processes of differentiation and dedifferentiation witness a drastic and dynamic alteration in the morphology, number, distribution, and respiratory capacity of mitochondria, which are tightly regulated by the fission/fusion cycle, and mitochondrial clearance through autophagy following mitochondrial fission. Intriguingly, mitophagy is said to be essential in the differentiation of stem cells into various lineages such as erythrocytes, eye lenses, neurites, myotubes, and M1 macrophages. Mitophagy is also believed to play a central role in the dedifferentiation of a terminally differentiated cell into an induced pluripotent cell and in the acquisition of 'stemness' in cancer cells. Mitophagy-induced alteration in the mitochondrial dynamics facilitates metabolic shift, either into a glycolytic phenotype or into an OXPHOS phenotype, depending on the cellular demand. Mitophagy-induced rejuvenation of mitochondria regulates the transition of bioenergetics and metabolome, remodeling which facilitates an alteration in their cellular developmental capability. This review describes the detailed mechanism of the process of mitophagy and its association with cellular programming through alteration in the mitochondrial energetics. The metabolic shift post mitophagy is suggested to be a key factor in the cell fate transition during differentiation and dedifferentiation.

Identifiants

pubmed: 30267101
doi: 10.1007/s00018-018-2922-9
pii: 10.1007/s00018-018-2922-9
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

27-43

Subventions

Organisme : DBT India Alliance
ID : BT/PR7791/BRB/10/1187/2013
Organisme : Board of Research in Nuclear Sciences
ID : 37(1)/14/38/2016-BRNS/37276
Organisme : Science and Engineering Research Board
ID : EMR/2016/001246

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Auteurs

Prajna Paramita Naik (PP)

Department of Life Science, National Institute of Technology Rourkela, Rourkela, Odisha, 769008, India.
P.G. Department of Zoology, Vikram Deb (Auto) College, Jeypore, Odisha, 764001, India.

Alexander Birbrair (A)

Department of Pathology, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.

Sujit Kumar Bhutia (SK)

Department of Life Science, National Institute of Technology Rourkela, Rourkela, Odisha, 769008, India. sujitb@nitrkl.ac.in.

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