AgingResearch.NewsJoin free
Cell Biology and Toxicology

Lowering a protein improved heart relaxation in aged mice

Mice given a heart-cell-targeted gene-silencing injection at 90 weeks had less inflammation and better heart relaxation when assessed at 110 weeks.

Paper by Wei Yang, Yuling Xu, Mingjian Jiang, +6 more authorsLin Yang
Figure 1 from Cell Biology and Toxicology
Open the figure at full size
Figure 1. Yang et al., CC BY-NC-ND

Our read

Mechanisms
Studied:
Experiments in naturally aged mice of both sexes
What changed:
Lowering TRAF1 improved heart relaxation in aged mice
The catch:
Heart relaxation was inferred from E/A and E/e′ ratios

Editor of record: Boris Djordjevic · AgingResearch.News

Paper
Follow @agingbrief

Naturally aged C57BL/6J mice of both sexes received a gene-silencing injection at 90 weeks that lowered TRAF1, a signaling protein, specifically in heart muscle cells. The animal experiment assessed their hearts at 110 weeks. Lowering TRAF1 reduced heart enlargement, inflammation and levels of reactive oxygen molecules. It improved diastolic function—how the heart relaxes and fills—but did not change ejection fraction, the share of blood pumped out with each beat.

In primary heart muscle cells treated with D-galactose in the lab, lowering TRAF1 reduced senescence, a state in which cells stop dividing, and reactive oxygen buildup. Increasing TRAF1 worsened these changes. In the cell experiments, TRAF1 promoted release of DNA from mitochondria, the cells’ energy-producing structures. This released DNA activated inflammatory signaling in macrophages, a type of immune cell.

Why it matters

Heart failure is an age-associated disease. The authors suggest that targeting TRAF1 may offer a strategy against age-related heart dysfunction.

Caveats

The heart-function findings came from a gene-silencing experiment in aged mice. They do not show whether lowering TRAF1 would help older people with heart failure.

Where the evidence stands

Inflammation

Cells, worms or flies, mice and humans: replicated by independent labs.

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

Against: findings that point the other way from most findings on the same outcome.

Company ties: findings with an author at a company, or from a paper whose competing-interests statement declares ties to one.

Includes the processes named after it and trials of drugs aimed at it.

  • 1,052 independent labs in 77 countries
  • 206 findings against
  • Funders: National Natural Science Foundation of China and others
  • 384 of 4,637 findings with company ties

TRAF1

Cells: a single group. Worms or flies, mice and humans: nothing yet.

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Includes the processes named after it and trials of drugs aimed at it.

  • 1 lab

Comments

Be the first to comment.

The paper

TRAF1 promotes age-related cardiac dysfunction through a three-step mechanism: cardiomyocyte senescence, mitochondrial DNA release, and subsequent macrophage-driven inflammation

Wei Yang, Yuling Xu, Mingjian Jiang, +6 more authorsLin Yang

Cell Biology and Toxicology, Nov 13, 2026, CC BY-NC-ND

doi.org/10.1007/s10565-026-10308-7

More on Inflammation