Breaking Update: Here’s a clear explanation of the latest developments related to Breaking News:Protein Prevents Cardiac Cellular Senescence – EMJ– What Just Happened and why it matters right now.
CARDIAC cellular senescence was significantly reduced by the matricellular protein CCN5 in new preclinical research, highlighting a potential therapeutic strategy for cardiovascular diseases (CVD).
CVD remains the leading cause of global mortality, with ageing and cumulative cellular stress central to disease progression. Cellular senescence, a state in which cells permanently stop dividing and adopt a pro-inflammatory profile, has been increasingly implicated in the pathogenesis of CVD. Identifying molecules capable of limiting cardiac cellular senescence has therefore become a major research priority.
In the new study, researchers investigated whether CCN5 (also known as WISP2), previously recognised for its anti-fibrotic effects in the heart, could directly modulate cardiac cellular senescence. Experiments were conducted in H9c2 cardiac myoblasts and cardiac fibroblasts using three established senescence markers: p53 and p21 protein expression, senescence-associated β-galactosidase staining, and γH2AX foci formation, a marker of DNA damage.
CCN5 Protein Suppresses Cardiac Cellular Senescence
The team demonstrated that CCN5 effectively inhibited doxorubicin-induced cardiac cellular senescence in both cardiac myoblasts and fibroblasts. Doxorubicin, a chemotherapeutic agent known to cause cardiotoxicity, is widely used to model stress-induced premature ageing in cardiac cells.
Importantly, CCN5 also disrupted the senescence-associated secretory phenotype (SASP), a pro-inflammatory signalling cascade through which senescent cells promote dysfunction in neighbouring tissue. When cardiac fibroblasts secreted SASP factors that induced senescence in myoblasts, CCN5 suppressed this cross-talk, and vice versa. These findings suggested that CCN5 not only acted within individual cells but also mitigated harmful intercellular signalling that amplified cardiac cellular senescence.
Restoring Apoptosis and Limiting Post-Infarction Senescence
Beyond preventing senescence, CCN5 restored the apoptotic response in senescent cells, potentially enabling the clearance of damaged cells that would otherwise persist in cardiac tissue. In a mouse model of myocardial infarction, CCN5 administration attenuated infarction-induced cardiac cellular senescence, supporting its relevance in vivo.
While the findings were limited to experimental models and require validation in human studies, they provide compelling evidence that CCN5 may serve as a dual anti-fibrotic and anti-senescence therapy. Future research will need to clarify optimal dosing, delivery strategies, and long-term safety.
If translated clinically, targeting cardiac cellular senescence with CCN5 could represent a novel approach to slowing structural remodelling and functional decline in CVD.
Reference
Jo Y et al. The matricellular protein CCN5 (WISP2) inhibits cellular senescence in cardiac myoblasts and fibroblasts. Sci Rep. 2026; doi:10.1038/s41598-026-40206-1.