Related Experiment Video
Updated: Apr 17, 2026
08:34
Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
15.9K
MARCH1 Deletion Attenuates HFpEF by Promoting Adipose Beiging
Yunlong Zhu1,2, Jie Fan2, Liang Tang1
1Department of Cardiology, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Comprehensive Physiology
|April 15, 2026
Summary
Membrane-associated RING-CH1 (MARCH1) inhibition improves heart failure with preserved ejection fraction (HFpEF) by reducing cardiac fibrosis and promoting white adipose tissue (WAT) beiging. Targeting MARCH1 and KLF15 offers potential new therapies for HFpEF.
Area of Science:
- Cardiology
- Metabolic Diseases
- Molecular Biology
Background:
- Membrane-associated RING-CH1 (MARCH1) is an E3 ubiquitin ligase involved in immune and metabolic functions.
- The role of MARCH1 in heart failure with preserved ejection fraction (HFpEF) pathogenesis is not well understood.
Purpose of the Study:
- To investigate the function of MARCH1 in a mouse model of HFpEF.
- To explore the therapeutic potential of targeting MARCH1 in HFpEF.
Main Methods:
- Established a multi-hit HFpEF mouse model using wild-type and MARCH1 knockout (KO) mice.
- Evaluated cardiac function via echocardiography and histology.
- Assessed white adipose tissue (WAT) beiging and molecular mechanisms using RNA sequencing and co-immunoprecipitation.
Main Results:
- HFpEF mice exhibited cardiometabolic dysregulation, cardiac fibrosis, and diastolic dysfunction.
- MARCH1 expression was upregulated in WAT of HFpEF mice.
- MARCH1 deficiency alleviated cardiac dysfunction, induced WAT beiging, and involved direct binding to KLF15.
Conclusions:
- MARCH1 inhibition demonstrates anti-fibrotic effects and promotes WAT beiging in HFpEF.
- Targeting MARCH1 and KLF15 presents a potential therapeutic strategy for HFpEF.
