Noncoding RNAs Controlling Telomere Homeostasis in Senescence and Aging

Aging is a universal and time-dependent biological decline associated with progressive deterioration of cells, tissues, and organs. Age-related decay can eventually lead to pathology such as cardiovascular and neurodegenerative diseases, cancer, and diabetes. A prominent molecular process underlying...

Full description

Saved in:
Bibliographic Details
Published in:Trends in molecular medicine Vol. 26; no. 4; pp. 422 - 433
Main Authors: Rossi, Martina, Gorospe, Myriam
Format: Journal Article
Language:English
Published: England Elsevier Ltd 01.04.2020
Subjects:
ISSN:1471-4914, 1471-499X, 1471-499X
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Aging is a universal and time-dependent biological decline associated with progressive deterioration of cells, tissues, and organs. Age-related decay can eventually lead to pathology such as cardiovascular and neurodegenerative diseases, cancer, and diabetes. A prominent molecular process underlying aging is the progressive shortening of telomeres, the structures that protect the ends of chromosomes, eventually triggering cellular senescence. Noncoding (nc)RNAs are emerging as major regulators of telomere length homeostasis. In this review, we describe the impact of ncRNAs on telomere function and discuss their implications in senescence and age-related diseases. We discuss emerging therapeutic strategies targeting telomere-regulatory ncRNAs in aging pathology. Senescent cells accumulating in aging tissues display indefinite cell cycle arrest, shortened telomeres, and enhanced secretion of proinflammatory factors.ncRNAs critically regulate gene expression programs in many physiological and pathological processes, including those associated with aging.ncRNAs regulate telomere homeostasis, either directly or indirectly, and thereby coordinate molecular processes inherent to cellular senescence and aging.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
ISSN:1471-4914
1471-499X
1471-499X
DOI:10.1016/j.molmed.2020.01.010