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Updated: Mar 1, 2026
A Simple and Efficient Method for In Vivo Cardiac-specific Gene Manipulation by Intramyocardial Injection in Mice
Published on: April 16, 2018
Farnesoid X receptor deletion improves cardiac function, structure and remodeling following myocardial infarction in
Jianshu Gao1, Xiaoqiang Liu2, Bingjian Wang3
1Department of Cardiology, Shanghai General Hospital of Nanjing Medical University, Shanghai 200080, P.R. China.
Abstract:
The farnesoid X receptor (FXR) is implicated in cholesterol and bile acid homeostasis; however, its role following myocardial infarction (MI) has yet to be elucidated. The aim of the present study was to investigate the effects of FXR knockout on left ventricular (LV) remodeling following MI. Coronary arteries of wild type (WT) and FXR‑/‑ mice were permanently occluded to cause MI, and serial echocardiographic and histological tests were conducted. At 4 weeks post‑MI, FXR‑/‑ mice exhibited significantly smaller infarct sizes (34.20±2.58 vs. 44.20±3.19%), improved ejection fraction (47.31±1.08 vs. 37.64±0.75%) and reduced LV chamber dilation compared with WT mice. LV remodeling was significant as early as 7 days post‑MI in FXR‑/‑ compared with WT mice. Histological features associated with enhanced long‑term remodeling and improved functionality, such as increased angiogenesis via detection of CD31 and reduced fibrosis, were observed in the FXR‑/‑ group. Myocyte apoptosis within the infarcted zones appeared significantly reduced by day 7 in FXR‑/‑ mice. In conclusion, the results of the present study suggested that FXR knockout may participate in the preservation of post‑MI cardiac functionality, via reducing fibrosis and chronic apoptosis, and ameliorating ventricular function.
Insights
Farnesoid X receptor (FXR) knockout preserves cardiac function after myocardial infarction (MI) by reducing fibrosis and apoptosis, leading to improved ventricular remodeling and ejection fraction in mice.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Receptor Signaling
Background:
- The farnesoid X receptor (FXR) regulates cholesterol and bile acid homeostasis.
- The role of FXR in cardiac remodeling following myocardial infarction (MI) remains unclear.
Purpose of the Study:
- To investigate the impact of FXR knockout on left ventricular (LV) remodeling post-MI.
- To elucidate the mechanisms by which FXR influences cardiac function after ischemic injury.
Main Methods:
- Myocardial infarction was induced in wild-type (WT) and FXR knockout (FXR-/-) mice via coronary artery occlusion.
- Serial echocardiography and histological analyses were performed to assess cardiac function and structure.
- Assessment of infarct size, ejection fraction, LV chamber dilation, angiogenesis (CD31), fibrosis, and myocyte apoptosis.
Main Results:
- FXR-/- mice showed significantly smaller infarct sizes and improved ejection fraction at 4 weeks post-MI compared to WT mice.
- Reduced LV chamber dilation and enhanced angiogenesis were observed in FXR-/- mice.
- Histological analysis revealed decreased fibrosis and significantly reduced myocyte apoptosis by day 7 in FXR-/- mice, indicating accelerated healing and preserved function.
Conclusions:
- FXR knockout ameliorates adverse LV remodeling and preserves cardiac function following MI.
- FXR deficiency may protect the heart by reducing chronic apoptosis and fibrosis in the infarcted area.
- Targeting FXR could be a potential therapeutic strategy for post-MI recovery.
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