Evidence map›Paper›PMID 42333952›Full record

ArticleAging cell2026

A Non-Channel Function of CFTR: Attenuating Mitochondrial Oxidative Stress and Cardiomyocyte Senescence via Stabilization by USP45.

Chun Chen, Longtan Jiang, Yuewen Qiu, Chong Liu, Xiao Long, Pengcui Wu, Liang Li, Haixia Xu, Ping Deng, Li Yang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Chun ChenDepartment of Cardiovascular Medicine, Hengyang Medical School, The Changsha Central Affiliated Hospital, University of South China, Changsha, China.
Longtan JiangDepartment of Cardiac Surgery, Xiangya Hospital, Central South University, Changsha, China.
Yuewen QiuDepartment of Ultrasound Medicine, The Changsha Central Affiliated Hospital, Hengyang Medical School, University of South China, Changsha, China.
Chong LiuDepartment of Cardiovascular Medicine, Hengyang Medical School, The Changsha Central Affiliated Hospital, University of South China, Changsha, China.
Xiao LongDepartment of Cardiovascular Medicine, Hengyang Medical School, The Changsha Central Affiliated Hospital, University of South China, Changsha, China.
Pengcui WuDepartment of Cardiovascular Medicine, Hengyang Medical School, The Changsha Central Affiliated Hospital, University of South China, Changsha, China.
Liang LiDepartment of Cardiovascular Medicine, Hengyang Medical School, The Changsha Central Affiliated Hospital, University of South China, Changsha, China.
Haixia XuDepartment of Medical Imaging, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, China.
Ping DengDepartment of Cardiovascular Medicine, Hengyang Medical School, The Changsha Central Affiliated Hospital, University of South China, Changsha, China.
Li YangDepartment of Cardiovascular Medicine, The Affiliated Zhuzhou Hospital Xiangya Medical College, Central South University, Zhuzhou, China.
Qiao JinDepartment of Cardiovascular Medicine, Hengyang Medical School, The Changsha Central Affiliated Hospital, University of South China, Changsha, China.ORCID https://orcid.org/0009-0008-3534-765X

Funding

Natural Science Foundation of Changsha City kq2502323Natural Science Foundation of Hunan Province 2025JJ80555Natural Science Foundation of Hunan Province 2025JJ80562Natural Science Foundation of Hunan Province 2026JJ30184Natural Science Foundation of Hunan Province 2026JJ81629
6 · The paper itself

Abstract

Cardiomyocyte senescence drives cardiovascular disease, underscoring the need to define its molecular mechanisms. The role of cystic fibrosis transmembrane conductance regulator (CFTR) ion channel in this process remains unclear, particularly regarding its expression and function. Atrial tissues were collected from patients with sinus rhythm or atrial fibrillation (AF) of varying durations. CFTR was downregulated in AF patients and negatively correlated with p16, p21, and p53. Myocardial aging models were established using D-galactose (D-gal) in both mice and neonatal mouse cardiomyocytes (CMs). In both animal and cellular models, D-gal increased SA-β-gal positivity and senescence markers while decreasing CFTR. Overexpressing CFTR reduced D-gal-induced elevations in p16, p21, p53, and malondialdehyde (MDA), and restored superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) activities. Mechanistically, CFTR alleviates mitochondrial oxidative stress damage by enhancing plasma membrane Ca

Indexed as

Cellular SenescenceCystic Fibrosis Transmembrane Conductance RegulatorMitochondriaMyocytes, CardiacOxidative StressAnimalsHumansMiceCystic Fibrosis Transmembrane Conductance Regulatorcardiomyocyte senescenceCFTRmitochondrial oxidative stressUSP45

Identifiers

PMID42333952
PMCPMC13288055

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.