Mitochondrial dynamics is required to adapt the manifold functions of mitochondria to cell needs and regulate their turnover by mitophagy. Actually, only if fragmented, mitochondria are engulfed by phagophores, the precursors to autophagosomes, and subsequently degraded. This process is essential to maintain a correct and healthy number of mitochondria that, otherwise, might be harmful. They, indeed, represent the main source of reactive oxygen species that - according to the mitochondrial free radical theory of aging - can cause aging when chronically overproduced. In a recent study, we demonstrated that S-nitrosylation, the reversible modification of cysteine residues by nitric oxide (NO), hyperactivates mitochondrial fragmentation by targeting DNM1L/Drp1 (dynamin 1-like) at Cys644, but inhibits mitophagy, the concomitant occurrence of these conditions driving cell senescence. We demonstrated that cell senescence, as well as mouse and human aging are characterized by an epigenetically-driven decrease in ADH5/GSNOR (alcohol dehydrogenase 5 [class III], chi polypeptide), suggesting that ADH5 may act as new longevity gene.

Rizza, S., Filomeni, G. (2018). Denitrosylate and live longer: how ADH5/GSNOR links mitophagy to aging. AUTOPHAGY, 14(7), 1285-1287 [10.1080/15548627.2018.1475818].

Denitrosylate and live longer: how ADH5/GSNOR links mitophagy to aging

RIZZA, SALVATORE;Filomeni, Giuseppe
2018-01-01

Abstract

Mitochondrial dynamics is required to adapt the manifold functions of mitochondria to cell needs and regulate their turnover by mitophagy. Actually, only if fragmented, mitochondria are engulfed by phagophores, the precursors to autophagosomes, and subsequently degraded. This process is essential to maintain a correct and healthy number of mitochondria that, otherwise, might be harmful. They, indeed, represent the main source of reactive oxygen species that - according to the mitochondrial free radical theory of aging - can cause aging when chronically overproduced. In a recent study, we demonstrated that S-nitrosylation, the reversible modification of cysteine residues by nitric oxide (NO), hyperactivates mitochondrial fragmentation by targeting DNM1L/Drp1 (dynamin 1-like) at Cys644, but inhibits mitophagy, the concomitant occurrence of these conditions driving cell senescence. We demonstrated that cell senescence, as well as mouse and human aging are characterized by an epigenetically-driven decrease in ADH5/GSNOR (alcohol dehydrogenase 5 [class III], chi polypeptide), suggesting that ADH5 may act as new longevity gene.
2018
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore BIO/10 - BIOCHIMICA
English
ADH5; Drp1; GSNOR; S-nitrosylation; Tet1; aging; cell senescence; mitochondrial dynamics; mitophagy; nitric oxide
https://www.tandfonline.com/doi/abs/10.1080/15548627.2018.1475818?journalCode=kaup20
Rizza, S., Filomeni, G. (2018). Denitrosylate and live longer: how ADH5/GSNOR links mitophagy to aging. AUTOPHAGY, 14(7), 1285-1287 [10.1080/15548627.2018.1475818].
Rizza, S; Filomeni, G
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/207529
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