Scientific reportsJun 29, 2026

Stem cells may prevent early aging-like changes in airway cells caused by cigarette smoke through a cell repair pathway

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗OA ↗

Updated Jun 30, 2026

Abstract

Umbilical cord mesenchymal stem cells (UC-MSCs) can improve mitochondrial dysfunction in bronchial epithelial cells caused by cigarette smoke exposure.

Cigarette smoke extract (CSE) causes mitochondrial dysfunction and an increase in reactive oxygen species (ROS), leading to cellular senescence.
UC-MSCs activate the SIRT1/PGC-1α pathway, which is associated with improved mitochondrial function and reduced cellular senescence markers following CSE exposure.
The protective effects of UC-MSCs are reversed by the SIRT1 inhibitor EX527, indicating the importance of this pathway.
The findings suggest a potential new target for treating chronic obstructive pulmonary disease (COPD) by addressing mitochondrial dysfunction.

Simplified

Chronic obstructive pulmonary disease (COPD) is an age-related chronic disease, and most of the patients are elderly. Smoking is the main pathogenic factor, and the course of disease continues to develop. Cigarette smoke exposure leads to mitochondrial dysfunction and activation of cellular senescence. Umbilical cord mesenchymal stem cells (UC-MSCs) play a significant role in mitochondrial protection, airway repair and tissue regeneration.SIRT1/PGC-1α is a key regulator of mitochondrial function and cellular senescence. Therefore, this study aims to explore whether UC-MSCs can improve cigarette smoke extract (CSE)-induced mitochondrial dysfunction and cellular senescence in bronchial epithelial cells by activating the SIRT1/PGC-1α pathway. In vitro results show that: (1) CSE induced mitochondrial dynamic imbalance, leading to mitochondrial dysfunction and ROS accumulation, which induced cellular senescence. (2) UC-MSCs activate the SIRT1/PGC-1α pathway and significantly reduce the expression of markers related to cellular senescence and improving mitochondrial function after CSE induction. (3) The SIRT1 inhibitor EX527 reversed the protective effect of UC-MSCs. This study, for the first time, reveals that UC-MSCs can improve CSE-induced mitochondrial dysfunction and cellular senescence in bronchial epithelial cells by activating the SIRT1/PGC-1α pathway. It provides a new target for COPD treatment and a strategy for slowing the progression of the disease.

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Funding

Competing interests

Declarations. Competing interests: The authors declare no competing interests.

PubMed

Stem cells may prevent early aging-like changes in airway cells caused by cigarette smoke through a cell repair pathway

Abstract

Full Text

Funding

Competing interests

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