FGD5-AS1 downregulates miR-129-5p levels to promote cardiomyocyte injury and apoptosis, accelerating the progression of chronic heart failure
4 affiliations
- 1Department of Cardiology, The First Hospital of Longyan, Longyan, 364000 China
- 2Department of Cardiovascular Medicine, Yantai Yantaishan Hospital, Yantai, 264000 China
- 3Department of Cardiology, Qingdao Municipal Hospital, Qingdao, 266011 China
- 4Department of Cardiovascular Medicine, The Affiliated Ganzhou Hospital of Nanchang University, No. 17 Hongqi Avenue, Zhanggong District, Ganzhou, 341000 Jiangxi China
Abstract
Background: Chronic heart failure (CHF) has a poor prognosis. LncRNA FGD5-AS1 and miR-129-5p play a key role in regulating cardiovascular diseases. This study aims to explore the clinical value and potential regulatory mechanisms of both in CHF.
Methods: The cell injury model was constructed in vitro using AC16 cells treated with DOX. The expressions of FGD5-AS1, miR-129-5p, and Bax, Bcl-2, and Caspase-3 were detected by RT-qPCR. The diagnostic and prognostic value of FGD5-AS1 was evaluated by ROC and Kaplan-Meier curves. CCK-8 and flow cytometry were used to assess cell proliferation and apoptosis. ELISA was used to detect the contents of inflammatory factors, ANP and BNP. The oxidative stress indicators SOD and MDA were detected by commercial kits.
Results: In patients with CHF, FGD5-AS1 and RUNX1 were upregulated, while miR-129-5p expression was downregulated. FGD5-AS1 has a good diagnostic value for patients with CHF. High levels of FGD5-AS1 are associated with a low survival rate in patients with CHF. Knockdown of FGD5-AS1 can increase the level of miR-129-5p, thereby alleviating Dox-induced cell proliferation inhibition, intensified apoptosis, oxidative stress (reducing MDA and increasing SOD), and overexpression of ANP/BNP.
Conclusions: FGD5-AS1 can sponge miR-129-5p and thereby up-regulate RUNX1 expression, which may be involved in the progression of CHF. It is an independent risk factor for poor prognosis in patients with CHF. FGD5-AS1 is expected to become a novel prognostic biomarker and potential therapeutic target for CHF.
Related
- Cannabidiol selectively downregulates FAM111B expression and induces apoptosis in fibrosarcoma cells: an in vitro study.
- PP2Acα deficiency attenuates doxorubicin-induced cardiac injury by suppressing cardiomyocyte apoptosis
- Glucocorticoids reprogram human AML leukemic stem cells to promote elimination through differentiation and apoptosis
- Epigallocatechin gallate and thermal cycling-stimulation synergistically promote apoptosis in A549 cells via endoplasmic reticulum stress-induced calcium ion dysregulation and oxidative stress
- CST1 stabilizes GPX4 to suppress ferroptosis and promote bladder cancer progression
BibTeX
@article{lin2026fgd5as1,
title = {{FGD5-AS1 downregulates miR-129-5p levels to promote cardiomyocyte injury and apoptosis, accelerating the progression of chronic heart failure}},
author = {Rongwen Lin and Jinhe Chen and Zhiying He and Jingwei Zheng},
journal = {Journal of Cardiothoracic Surgery},
year = {2026},
month = jul,
doi = {10.1186/s13019-026-04619-3},
url = {https://doi.org/10.1186/s13019-026-04619-3},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - FGD5-AS1 downregulates miR-129-5p levels to promote cardiomyocyte injury and apoptosis, accelerating the progression of chronic heart failure
AU - Rongwen Lin
AU - Jinhe Chen
AU - Zhiying He
AU - Jingwei Zheng
PY - 2026
DA - 2026/07/29
JO - Journal of Cardiothoracic Surgery
DO - 10.1186/s13019-026-04619-3
UR - https://doi.org/10.1186/s13019-026-04619-3
AB - Background: Chronic heart failure (CHF) has a poor prognosis. LncRNA FGD5-AS1 and miR-129-5p play a key role in regulating cardiovascular diseases. This study aims to explore the clinical value and potential regulatory mechanisms of both in CHF. Methods: The cell injury model was constructed in vitro using AC16 cells treated with DOX. The expressions of FGD5-AS1, miR-129-5p, and Bax, Bcl-2, and Caspase-3 were detected by RT-qPCR. The diagnostic and prognostic value of FGD5-AS1 was evaluated by ROC and Kaplan-Meier curves. CCK-8 and flow cytometry were used to assess cell proliferation and apoptosis. ELISA was used to detect the contents of inflammatory factors, ANP and BNP. The oxidative stress indicators SOD and MDA were detected by commercial kits. Results: In patients with CHF, FGD5-AS1 and RUNX1 were upregulated, while miR-129-5p expression was downregulated. FGD5-AS1 has a good diagnostic value for patients with CHF. High levels of FGD5-AS1 are associated with a low survival rate in patients with CHF. Knockdown of FGD5-AS1 can increase the level of miR-129-5p, thereby alleviating Dox-induced cell proliferation inhibition, intensified apoptosis, oxidative stress (reducing MDA and increasing SOD), and overexpression of ANP/BNP. Conclusions: FGD5-AS1 can sponge miR-129-5p and thereby up-regulate RUNX1 expression, which may be involved in the progression of CHF. It is an independent risk factor for poor prognosis in patients with CHF. FGD5-AS1 is expected to become a novel prognostic biomarker and potential therapeutic target for CHF.
SN - 1749-8090
ER -