CD47 blockade reduces doxorubicin-induced cardiac aging in male mice
Inhibiting CD47 lessens heart dysfunction and blunts cellular senescence caused by the chemotherapy drug doxorubicin.
Physiological reports · Yan A et al. · Paper published 1 Sep 2026
In male mice and cultured AC16 cardiomyocytes, researchers examined how CD47 regulates chemotherapy-induced cardiac aging. Initial bioinformatic analyses revealed that CD47 increases in aged hearts. The team then treated mice with doxorubicin, which raised CD47 expression alongside senescence markers p53, p16, and p21 in heart tissue. In AC16 cells, doxorubicin similarly boosted CD47 levels, p16, p21, and senescence-associated beta-galactosidase activity. Blocking CD47 with a specific antibody reduced cardiomyocyte senescence both in vitro and in vivo. Furthermore, CD47 inhibition improved doxorubicin-induced cardiac dysfunction in the animals.
Why it matters
Anticancer therapies frequently accelerate cardiac aging and functional decline. Identifying CD47 as a mediator of this process reveals a mechanistic link between therapy-induced stress and tissue senescence.
Caveats
The findings rely on cultured cells and male mice rather than human patients. Further work is needed to determine whether these effects translate across sexes and into clinical settings.
Written from the paper’s abstract, and every claim checked against it before publishing. Read the paper for the full methods and data.
The paper
CD47 is a regulator in doxorubicin-induced cardiac aging in male mice
Yan A, Mai R, Cao T et al.
Physiological reports · 1 Sep 2026 · Peer-reviewed
- Relevance
- Core geroscience
- News value
- Notable
- Evidence
- Animals
- Status
- Peer-reviewed
More on Cellular senescence
See allDasatinib and quercetin reduce liver fibrosis in a phase-2 MASH trial
The senolytic combination improved liver fibrosis without disease worsening in nearly half of treated participants while lowering cellular senescence markers.
Nature metabolism · Koning M et al.
A distinct p21-driven macrophage senotype accumulates during aging and liver disease
Researchers identified a p53-p21-Cyclin D2 axis that governs senescent macrophages in mice and human liver cirrhosis and can be cleared with senolytics.
bioRxiv · Torres G et al.
DNA methylation proxies of senescence markers track human disease and mortality
The new blood-based tools estimate senescence gene activity to predict incident diseases, all-cause mortality, and clinical treatment responses.
medRxiv · Simpson DJ et al.
Bispecific T cell engager eliminates senescent cells in mice and nonhuman primates
Monitored by serum transaminase levels, low doses of the drug alleviated age-related pathologies without causing the hepatotoxicity seen at higher doses.
Aging cell · Deng J et al.
A deep learning score for cellular senescence predicts human mortality and disease risk
The proteomic biomarker tracked chronic illness risk in the UK Biobank and shifted following an 18-month multimodal exercise intervention.
Aging cell · Zhao S et al.