A Signature Of Senescence Based On An Analysis Of Selected Markers In Primary Vascular Smooth Muscle Cells Cultured In Vitro And Derived From Atherosclerotic Plaque
Our bodies are constantly renewing cells, but sometimes cells enter a state called “senescence,” where they stop dividing but remain active. These senescent cells can accumulate in tissues and contribute to aging-related diseases, including atherosclerosis, a condition where plaque builds up inside arteries. Pinpointing these senescent cells has been a challenge because their characteristics can vary widely depending on the cell type and what caused them to become senescent. This makes it difficult to study their role in disease and develop targeted treatments.
Recent research focused on vascular smooth muscle cells (VSMCs), which are key players in the development of atherosclerosis. By studying VSMCs both grown in the lab and isolated from human atherosclerotic plaques, scientists have identified a consistent set of markers that reliably indicate when these cells are senescent. They found that changes in certain nuclear proteins, like Lamin B1, HMGB1, and PARP1, were particularly stable indicators of senescence. While other common senescence markers, such as p53, p21, and p16, showed some variability, the identified nuclear protein changes provided a robust “signature” for senescent VSMCs. This breakthrough offers a more confident way to identify and study these cells, regardless of how or when they became senescent, paving the way for a better understanding of their role in atherosclerosis and potentially new therapeutic strategies.
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