Cellular senescence may be to blame for some diseases

Cellular senescence is a process in which the cell cycle becomes permanently arrested, thereby inhibiting cell division, proliferation and growth. Various cellular stresses, such as DNA damage, telomere shortening and oxidative stress, can trigger cellular senescence. Physiologically, cellular senescence contributes to tissue development, repair and critical biological processes such as embryogenesis, whereas, pathologically, it plays a key role in diverse conditions, including age-related disease, some cancers, Alzheimer’s disease, and others.

A paper titled “Hallmarks of cellular senescence: biology, mechanisms, regulations,” published in Experimental & Molecular Medicine, explores recent key findings on cellular senescence in experimental and human disease models, focusing on its molecular mechanisms, regulation and future research directions to advance the field and facilitate therapeutic translation.

Overall, the authors note that cellular senescence serves as a stopwatch for the cell cycle under severe stress conditions, such as DNA damage, oxidative stress and telomere shortening. The physiological and pathological impacts of senescent cells are largely mediated by unknown mechanisms, and the translational relevance of current findings on cellular senescence remains limited. Therefore, further studies are required to address remaining questions and fill existing gaps.

The researchers provide insights into new research directions and potential bottlenecks for therapeutic intervention targeting cellular senescence in related conditions in order to further address all aspects of this process through additional experimental studies.

Domenico Praticò, MD, the Scott Richards North Star Foundation Chair for Alzheimer’s Research, Professor of Neural Sciences at the Alzheimer’s Center at Temple (ACT), in the Lewis Katz School of Medicine at Temple University (LKSOM), contributed to the paper as a co-author.

Provided by
Alzheimer’s Center at Temple University Lewis Katz School of Medicine