American journal of physiology. Cell physiologyJun 18, 2026

Cell aging as a control process in muscle healing in young mice

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Jun 19, 2026

Abstract

Macrophage infiltration was twice as high in the group treated with senolytics compared to the control group at D7.

The removal of senescent cells through senolytic treatment altered the dynamics of muscle repair in young mice.
There were no significant differences in functional measures like hindlimb grip strength or cross-sectional area between the treatment and control groups.
Elevated levels of muscle fibers expressing embryonic myosin heavy chain (eMHC) were observed in the senolytic treatment group at D28.
The quantity of satellite cells and fibrotic area were significantly increased at D14 in the senolytic treatment group compared to the control group.
Senescent cells may serve as a regulatory mechanism in skeletal muscle repair, influencing the activity of immune cells, satellite cells, and fibrotic cells.

Simplified

Senescence is broadly considered an age-related phenomenon; however, it also been implicated in normal tissue repair and wound healing. Skeletal muscle repair is a complex process that requires the coordination of several different cell populations but the role of senescence in skeletal muscle repair has yet to be fully elucidated. We hypothesize that senescence serves as a control mechanism throughout the regenerative process and the removal of senescent cells through senolytics will negatively impact the repair process in young mice. Briefly, young mice were exposed to either (a) vehicle (VEH), receiving only a cardiotoxin (CTx) injection in one hindlimb or (b) 7 days of senolytic treatment (SEN) pre-CTx and 3x/week for 4 weeks post-CTx. Dasatinib + Quercetin (D+Q) was used to selectively eliminate senescent cells. There were no significant differences between groups in functional measures such as hindlimb grip strength and cross-sectional area. eMHC+ fibers remained elevated at D28 in the SEN group. Macrophage infiltration was twice as high in the SEN group compared to VEH at D7. Satellite cell quantity and fibrotic area were significantly increased at D14 in the SEN group compared to VEH. We conclude that reducing senescent cells during muscle repair in young mice significantly altered the kinetics of muscle repair. Therefore, senescent cells may act as a regulatory mechanism in skeletal muscle to orchestrate the activity of the different cell populations involved in repair and regeneration such as immune cells, satellite cells, and fibrotic cells.

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Cell aging as a control process in muscle healing in young mice

Abstract

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