The authors investigate the physiological functions of Terc-53 by creating transgenic mice that overexpress this noncoding RNA. They observe that Terc-53 overexpression affects normal aging in mammals, contributing to cognitive decline and shortened lifespan.
Higher Education PressAug 27 2024 Mechanistically, they find that Terc-53 binds to and promotes the degradation of Hmmr, leading to enhanced inflammation in tissues and accelerated aging. They also note that Hmmr levels decrease with age in certain brain regions, similar to Terc-53's pattern, and that restoring Hmmr levels can improve cognitive abilities and reduce neuroinflammation markers.
It demonstrates that Terc-53 regulates organismal aging through the stability of Hmmr and the modulation of neuroinflammation. The findings open new avenues for understanding and potentially treating age-related physical debilities and improving healthspan. By identifying Hmmr as a critical mediator of Terc-53's effects on aging, the research suggests that strategies aimed at stabilizing Hmmr could mitigate age-related cognitive decline and inflammation.
Receptor RNA Cell Inflammation Protein Research Transgenic
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