Blocking activin signals improved heart filling in mice
Removing two activin receptor types from certain immune cells lowered a heart-filling pressure index to 31.93, versus 42.99 in heart-failure mice.
Our read
Mechanisms- Studied:
- Experiments in male mice with induced HFpEF, 15-16 weeks, against mice with HFpEF
- What changed:
- Diastolic function improved, with E/E′ reaching 31.93±6.66 compared to 42.99±9.01 in HFpEF controls
- The catch:
- RKER-065 blocked multiple signaling proteins, so its effects cannot be attributed to activin alone
- Why it’s aging research:
- It studies something that builds up in the body with age.
Editor of record: Boris Djordjevic · AgingResearch.News
Male, 6-month-old C57BL6/J mice received a high-fat diet and the drug L-NAME for 15–16 weeks in an animal experiment. This modeled heart failure with preserved ejection fraction, in which the heart pumps out a normal share of its blood. Macrophages, a type of immune cell, predominated among cells carrying a marker of senescence, a state in which cells stop dividing.
Removing two types of receptor—proteins that receive signals—for activin, a circulating protein, from myeloid immune cells improved heart filling. The drug RKER-065 blocked several proteins that bind these receptors. It reduced senescence-related gene activity in heart macrophages, improved heart filling and exercise capacity, and reduced heart mass. Neither intervention changed body weight, body composition or blood pressure.
Why it matters
Heart failure with preserved ejection fraction is associated with aging and inflammation. The authors highlighted activin signaling as a promising therapeutic target for this condition.
Caveats
The results came from an induced heart-failure model in male mice and were reported in a conference abstract. RKER-065 blocked multiple signaling proteins, so its effects cannot be attributed to activin alone.
The paper
Stanley and Judith Frankel Institute for Heart and Brain Health
AHA Scientific Sessions 2026 Abstract, Nov 2, 2026
Presented at AHA Scientific Sessions 2026, abstract 15131
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