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Background <p>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.</p> Methods <p>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.</p> Results <p>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.</p> Conclusions <p>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.</p>

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FGD5-AS1 downregulates miR-129-5p levels to promote cardiomyocyte injury and apoptosis, accelerating the progression of chronic heart failure

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月29日

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  • Rongwen Lin,
  • Jinhe Chen,
  • Zhiying He,
  • Jingwei Zheng

摘要

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.