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A conserved KLF-autophagy pathway modulates nematode lifespan and mammalian age-associated vascular dysfunction.

Abstract：

:Loss of protein and organelle quality control secondary to reduced autophagy is a hallmark of aging. However, the physiologic and molecular regulation of autophagy in long-lived organisms remains incompletely understood. Here we show that the Kruppel-like family of transcription factors are important regulators of autophagy and healthspan in C. elegans, and also modulate mammalian vascular age-associated phenotypes. Kruppel-like family of transcription factor deficiency attenuates autophagy and lifespan extension across mechanistically distinct longevity nematode models. Conversely, Kruppel-like family of transcription factor overexpression extends nematode lifespan in an autophagy-dependent manner. Furthermore, we show the mammalian vascular factor Kruppel-like family of transcription factor 4 has a conserved role in augmenting autophagy and improving vessel function in aged mice. Kruppel-like family of transcription factor 4 expression also decreases with age in human vascular endothelium. Thus, Kruppel-like family of transcription factors constitute a transcriptional regulatory point for the modulation of autophagy and longevity in C. elegans with conserved effects in the murine vasculature and potential implications for mammalian vascular aging.KLF family transcription factors (KLFs) regulate many cellular processes, including proliferation, survival and stress responses. Here, the authors position KLFs as important regulators of autophagy and lifespan in C. elegans, a role that may extend to the modulation of age-associated vascular phenotypes in mammals.

journal_name

Nat Commun

journal_title

Nature communications

authors

Hsieh PN,Zhou G,Yuan Y,Zhang R,Prosdocimo DA,Sangwung P,Borton AH,Boriushkin E,Hamik A,Fujioka H,Fealy CE,Kirwan JP,Peters M,Lu Y,Liao X,Ramírez-Bergeron D,Feng Z,Jain MK

doi

10.1038/s41467-017-00899-5

subject

Has Abstract

pub_date

2017-10-13 00:00:00

pages

914

issue

1

issn

2041-1723

pii

10.1038/s41467-017-00899-5

journal_volume

8

pub_type

杂志文章

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