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. 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.
Key findings from the study include:
The study highlights the complexity of aging in mammals and the significance of noncoding RNAs and proteins that emerged late in evolution. 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. The work entitled “ Noncoding RNA Terc-53 and hyaluronan receptor Hmmr regulate aging in mice ” was published on Protein & Cell (published on May. 09, 2024).
Protein & Cell
Experimental study
Animals
Noncoding RNA Terc-53 and hyaluronan receptor Hmmr regulate aging in mice
9-May-2024