Endoplasmic reticulum stress-induced senescence in human lung fibroblasts-Reference-Cited by-同舟云学术

Endoplasmic reticulum stress-induced senescence in human lung fibroblasts

Published:2024-07-01 Issue:1 Volume:327 Page:L126-L139
ISSN:1040-0605
Container-title:American Journal of Physiology-Lung Cellular and Molecular Physiology
language:en
Short-container-title:American Journal of Physiology-Lung Cellular and Molecular Physiology

Author:

Koloko Ngassie Maunick Lefin¹²³^ORCID,Drake Li Y.³^ORCID,Roos Benjamin B.³,Koenig-Kappes Amanda³,Pabelick Christina M.³⁴^ORCID,Gosens Reinoud²⁵^ORCID,Brandsma Corry-Anke¹²^ORCID,Burgess Janette K.¹²^ORCID,Prakash Y. S.³⁴^ORCID

Affiliation:

1. Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands

2. Groningen Research Institute for Asthma and COPD, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands

3. Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, Minnesota, United States

4. Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, United States

5. Department of Molecular Pharmacology, University of Groningen, Groningen, The Netherlands

Abstract

The current study establishes functional links between endoplasmic reticulum (ER) stress and cellular senescence per se in the specific context of aging human lung fibroblasts. Recognizing that the process of aging per se is complex, modulated by the myriad of lifelong and environmental exposures, it is striking to note that chronic ER stress may play a crucial role in the establishment and maintenance of cellular senescence in lung fibroblasts.

Funder

HHS | NIH | National Heart, Lung, and Blood Institute

Nederlandse Organisatie voor Wetenschappelijk Onderzoek

Albert Tasman Talent Program Fellowship in association with Healthy Aging Alliance

Publisher

American Physiological Society

Link

https://journals.physiology.org/doi/pdf/10.1152/ajplung.00264.2023

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