Author: Xingjie Ma 1, Qingbin Zheng 2, Guangming Zhao 2, Wenjie Yuan 2, Weili Liu 3
Affiliation: 1 Department of Intensive Care, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, China; Department of the Central laboratory, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, China.
2 Department of Intensive Care, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, China.
3 Department of Intensive Care, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, China. Electronic address: zyyliuweili@126.com.
Conference/Journal: Mech Ageing Dev
Date published: 2020 May 22
Other:
Volume ID: 111264 , Word Count: 215
PMID: 32450085 DOI: 10.1016/j.mad.2020.111264
Abstract
Cellular senescence is mainly characterized as a stable proliferation arrest and a senescence associated secretory phenotype (SASP). Senescence is triggered by diverse stimuli such as telomere shortening, oxidative stress, oncogene activation and DNA damage, and consequently contributes to multiple physiology and pathology outcomes, including embryonic development, wound healing and tumor suppression as well as aging or age-associated diseases. Interestingly, therapeutic clearance of senescent cells in tissues has recently been demonstrated to be beneficial for extending a healthy lifespan and for improving numerous age-related disorders. However the molecular mechanisms of senescence regulation remain partially understood. Theoretically, senescence is tightly regulated by a vast number of molecules, among which the p16 and p53 pathways are the most classical. In addition, intracellular cellular calcium signaling has emerged as a key regulator of senescence. In the last few decades, a growing number of studies have demonstrated that microRNAs (miRNAs, small non-coding RNAs) are strongly implicated in controlling senescence, especially at the transcriptional and post-transcriptional levels. In this review we will discuss the involvement of miRNAs in modulating senescence through the major p16, p53, SASP and calcium signaling pathways, thus aiming to reveal the mechanisms of how miRNAs regulate cellular senescence.
Keywords: Calcium signaling; SASP; Senescence; miRNAs; p16/p53.
Copyright © 2020. Published by Elsevier B.V.