Creb3l1, a transcription factor that regulates collagen and structural protein production, restores mechanical strength and healing capacity in aged tendons when overexpressed. The finding connects epidemiological data showing increased tendon injury prevalence with age to a specific molecular mechanism responsible for age-related tendon deterioration, suggesting a targetable pathway for repair dysfunction.
Key Points
- Creb3l1 overexpression restores Col1a1 and Sparc expression in aged tendons
- Aged tendons show compromised mechanical properties and healing strength
- Single therapeutic target improves gliding function, healing strength, elastic modulus
Longevity Analysis
Tendon injury burden increases substantially with age despite declining incident rates, indicating that aging compromises tissue repair capacity rather than exposure. The identification of Creb3l1 as a regulatory hub for collagen and structural protein synthesis provides a concrete mechanism by which cellular signaling declines with age, and demonstrates that targeted restoration of gene expression can reverse mechanical degeneration in connective tissue. This work illustrates how understanding the molecular signals that govern tissue regeneration can lead to interventions that restore function in aged tissues — a principle relevant across musculoskeletal repair and broader regenerative capacity.
Original published by Wiley Aging Cell, by Qian Qian Yang, Zhanghao Huang, Yan Xue, Jia Yu Shi, You Lang Zhou .