Inhibition Of C-Jun/Bak Signaling Alleviates Endothelial Cell Senescence And Inflammation Caused By Mitochondrial Dysfunction In DMED
Our bodies’ blood vessels are lined with special cells called endothelial cells, which are crucial for maintaining a healthy circulatory system. However, these cells can age prematurely and become inflamed, particularly when their internal powerhouses, the mitochondria, malfunction. This mitochondrial dysfunction can lead to a cascade of problems, including reduced blood flow and conditions like diabetic erectile dysfunction. Recent research has identified a specific cellular pathway, involving molecules known as c-Jun and Bak, that contributes to this premature aging (senescence) and inflammation of endothelial cells. By blocking this pathway, it was observed that the detrimental effects of mitochondrial dysfunction on these vital blood vessel cells could be alleviated. This discovery opens up new avenues for developing treatments that could protect our blood vessels from age-related damage and inflammation, potentially improving conditions linked to impaired mitochondrial function.
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