# AEBP1 suppression improved cardiac function in mice and reversed remodeling in failing human heart tissue

- Published: 2026-11-07 15:55 UTC
- Section: Life & Health › Medicine
- Tags: AEBP1, ACLP, myocardial fibrosis, cardiac fibroblasts, heart failure, reverse remodeling, MRTFB, RUNX2, University of Utah, Nature Communications
- URL: https://realtech.media/news/rt-8e7a7e16f39e515bae9d43bb_aebp1_suppression_improved/

**University of Utah-led team found that the protein AEBP1 mediates myocardial fibrosis. Its knockout helped mouse hearts, and knockdown reversed remodeling in cultured failing human myocardium.**

![AEBP1 suppression improved cardiac function in mice and reversed remodeling in failing human heart tissue](https://realtech.media/media/2026/11/77bca20939eea11e.jpg)
*Hibiscus Rosa Sinensis, Wikimedia Commons, CC BY 4.0*

A research team from the University of Utah, Washington University School of Medicine and partner institutions reports that the protein AEBP1 mediates myocardial fibrosis and adverse cardiac remodeling. The study was published in Nature Communications on 6 November 2026. Experiments were carried out in mouse models and in cultured human myocardial tissue. [1]

Persistent activation of cardiac fibroblasts leads to excessive deposition of extracellular matrix. According to the authors, this promotes maladaptive myocardial fibrosis, adverse remodeling and progression of heart failure. AEBP1 and ACLP, the full-length protein it encodes, had been linked to pathological fibrosis in several organs, including the heart. Its functional role in cardiac fibrosis, however, remained unknown. [1]

## AEBP1 knockout in mice and human tissue culture

In mice, fibroblast-specific knockout of Aebp1, or knockdown of it in the myocardium, significantly improved cardiac function and prevented pathological remodeling. Two injury models were used: myocardial ischemia and pressure overload. [1]

In cultured human myocardial tissue, ACLP overexpression induced pathological remodeling in non-failing hearts. AEBP1 knockdown, in turn, induced structural reverse remodeling in failing myocardium. [1]

## Mechanism: MRTFB, RUNX2 and fibroblast activation

The authors report that ACLP regulates the expression of MRTFB, RUNX2, SM22 and COL1A1, and in this way orchestrates fibroblast activation. [1]

From these results the authors identify AEBP1 as a mediator of myocardial fibrosis. They describe its inhibition as a potential anti-fibrotic therapy after acute injury. The results reported here come from mouse models and human tissue culture. [1]

The work was done at the Nora Eccles Harrison Cardiovascular Research and Training Institute at the University of Utah, with participation of groups from Washington University in St. Louis, Friedrich-Alexander University Erlangen-Nuremberg and Boston University. The corresponding authors are Eleni Tseliou and Stavros G. Drakos. [1]

## Sources

1. [Nature Communications](https://doi.org/10.1038/s41467-026-79136-x)

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Source: RealTech, realtech.media — https://realtech.media/news/rt-8e7a7e16f39e515bae9d43bb_aebp1_suppression_improved/