Toward understanding genomic instability, mitochondrial dysfunction and aging
Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
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Toward understanding genomic instability, mitochondrial dysfunction and aging. / Fakouri, Nima B; Hou, Yujun; Demarest, Tyler G; Christiansen, Louise Slot; Okur, Mustafa N; Mohanty, Joy G; Croteau, Deborah L; Bohr, Vilhelm A.
I: F E B S Journal, Bind 286, Nr. 6, 2019, s. 1058-1073.Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
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TY - JOUR
T1 - Toward understanding genomic instability, mitochondrial dysfunction and aging
AU - Fakouri, Nima B
AU - Hou, Yujun
AU - Demarest, Tyler G
AU - Christiansen, Louise Slot
AU - Okur, Mustafa N
AU - Mohanty, Joy G
AU - Croteau, Deborah L
AU - Bohr, Vilhelm A
N1 - (Ekstern)
PY - 2019
Y1 - 2019
N2 - The biology of aging is an area of intense research, and many questions remain about how and why cell and organismal functions decline over time. In mammalian cells, genomic instability and mitochondrial dysfunction are thought to be among the primary drivers of cellular aging. This review focuses on the interrelationship between genomic instability and mitochondrial dysfunction in mammalian cells and its relevance to age-related functional decline at the molecular and cellular level. The importance of oxidative stress and key DNA damage response pathways in cellular aging is discussed, with a special focus on poly (ADP-ribose) polymerase 1, whose persistent activation depletes cellular energy reserves, leading to mitochondrial dysfunction, loss of energy homeostasis, and altered cellular metabolism. Elucidation of the relationship between genomic instability, mitochondrial dysfunction, and the signaling pathways that connect these pathways/processes are keys to the future of research on human aging. An important component of mitochondrial health preservation is mitophagy, and this and other areas that are particularly ripe for future investigation will be discussed.
AB - The biology of aging is an area of intense research, and many questions remain about how and why cell and organismal functions decline over time. In mammalian cells, genomic instability and mitochondrial dysfunction are thought to be among the primary drivers of cellular aging. This review focuses on the interrelationship between genomic instability and mitochondrial dysfunction in mammalian cells and its relevance to age-related functional decline at the molecular and cellular level. The importance of oxidative stress and key DNA damage response pathways in cellular aging is discussed, with a special focus on poly (ADP-ribose) polymerase 1, whose persistent activation depletes cellular energy reserves, leading to mitochondrial dysfunction, loss of energy homeostasis, and altered cellular metabolism. Elucidation of the relationship between genomic instability, mitochondrial dysfunction, and the signaling pathways that connect these pathways/processes are keys to the future of research on human aging. An important component of mitochondrial health preservation is mitophagy, and this and other areas that are particularly ripe for future investigation will be discussed.
KW - DNA damage
KW - Mitochondria
KW - Mitophagy
KW - NAD
KW - PARP
U2 - 10.1111/febs.14663
DO - 10.1111/febs.14663
M3 - Review
C2 - 30238623
AN - SCOPUS:85054485629
VL - 286
SP - 1058
EP - 1073
JO - F E B S Journal
JF - F E B S Journal
SN - 1742-464X
IS - 6
ER -
ID: 255883147