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Novel gene therapy CM-YAPon protects the mouse heart from myocardial infarction

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE293210 | GEO | 2025/09/30

REPOSITORIES: GEO

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Novel gene therapy CM-YAPon protects the mouse heart from myocardial infarction - MI

Project description:Myocardial infarction (MI), which affects about 3 million people globally each year, permanently damages the heart and reduces cardiac function1. Recent studies have indicated that activating YAP in cardiomyocytes (CMs) promotes cardiac regeneration and mitigates pathological remodeling in mouse and pig MI models2,3. To precisely control YAP activity in vivo and encourage its clinical application, we developed an adeno-associated virus 9 (AAV9)-based therapy, termed CM-YAPon, which triggers YAP activation in CMs upon exposure to a small molecule LMI070. One dose of LMI070 in mice induced a transient expression of active YAP (YAP5SA), which was subsequently degraded within a week. Consistent with earlier findings, YAP activation after injury improved cardiac function. Interestingly, administering a single LMI070 injection two weeks before MI provided lasting cardioprotection, which diminished by four weeks after the transient YAP activation, by reducing non-CMs cell death and enhancing cardiac function. Taken together, our novel gene therapy CM-YAPon presents a promising avenue for developing protective strategies against MI-induced cardiac injury.

2025-09-30 | GSE293327 | GEO

Novel gene therapy CM-YAPon protects the mouse heart from myocardial infarction - Virus Test

2025-09-30 | GSE270256 | GEO

Novel gene therapy CM-YAPon protects the mouse heart from myocardial infarction - 3 day post-LMI

2025-09-30 | GSE293209 | GEO

Novel gene therapy CM-YAPon protects the mouse heart from myocardial infarction

Project description:Novel gene therapy CM-YAPon protects the mouse heart from myocardial infarction

| PRJNA1243347 | ENA

Novel gene therapy CM-YAPon protects the mouse heart from myocardial infarction - MI

Project description:Novel gene therapy CM-YAPon protects the mouse heart from myocardial infarction - MI

| PRJNA1244144 | ENA

Novel gene therapy CM-YAPon protects the mouse heart from myocardial infarction - Virus Test

Project description:Novel gene therapy CM-YAPon protects the mouse heart from myocardial infarction - Virus Test

| PRJNA1125889 | ENA

Novel gene therapy CM-YAPon protects the mouse heart from myocardial infarction - 3 day post-LMI

Project description:Novel gene therapy CM-YAPon protects the mouse heart from myocardial infarction - 3 day post-LMI

| PRJNA1243356 | ENA

Multi-omics analysis of early reperfused ischemic heart reveals ERRβ/γ activation protects against acute myocardial infarction injury

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-08-01 | GSE240850 | GEO

Identification of Novel Serum Biomarkers for Early Decision of ST-elevation Myocardial Infarction

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-05-23 | E-GEOD-61145 | biostudies-arrayexpress

Mouse Mast Cell Protease 4 Deletion Protects Heart Function and Survival After Permanent Myocardial Infarction.

Project description:Chymase, a mast cell serine protease involved in the generation of multiple cardiovascular factors, such as angiotensin II and endothelin-1 (ET-1), is elevated and participates in tissue degeneration after permanent myocardial infarction (PMI). Anesthetized 4-month old male wild-type (WT) C57BL/6J mice and mouse mast cell protease-4 knockout (mMCP-4 KO) congeners were subjected to ligation of the left anterior descending (LAD) coronary artery. A group of mice was then subjected to Kaplan-Meier 28-day survival analysis. In another group of mice, 18F-fluorodeoxyglucose positron emission tomography (PET) was performed to evaluate heart function and the infarcted zone 3 days post-PMI surgery. Cardiac morphology following PMI was evaluated on formalin-fixed heart slices and glycoproteomic analysis was performed using mass spectrometry. Finally, cardiac and lung tissue content of immunoreactive ET-1 was determined. PMI caused 60% mortality in WT mice, due to left ventricular wall rupture, and 7% in mMCP-4 KO mice. Cardiac PET analysis revealed a significant reduction in left ventricular volume (systolic and diastolic) and preserved the ejection fraction in mMCP-4 KO compared to WT animals. The infarcted area, apoptotic signaling and wall remodeling were significantly decreased in mMCP-4 KO mice compared to their WT congeners, while collagen deposition was increased. Glycoproteomic analysis showed an increase in apolipoprotein A1, an established chymase substrate in mMCP-4 KO mice compared to WT mice post-PMI. ET-1 levels were increased in the lungs of WT, but not mMCP-4 KO mice, 24 h post-PMI. Thus, the genetic deletion of mMCP-4 improved survival and heart function post-PMI.

| S-EPMC6127244 | biostudies-literature

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