Cellular Senescence Mediates Doxorubicin Chemotherapy-Induced Vascular Endothelial Dysfunction: Translational Evidence Of Prevention With Senolytic Treatment
Chemotherapy, while crucial for fighting cancer, can sometimes have unwanted side effects on healthy tissues. One common chemotherapy drug, doxorubicin, is known to cause problems with our blood vessels, specifically a condition called vascular endothelial dysfunction. This means the inner lining of our blood vessels doesn’t function as it should, potentially leading to cardiovascular issues.
Recent investigations have shed light on a key mechanism behind this side effect: cellular senescence. Imagine some of your cells as “zombies” – they stop dividing, but they don’t die off. Instead, they linger, releasing substances that can harm neighboring healthy cells and tissues. This state is called cellular senescence.
This new work suggests that these senescent cells play a significant role in the blood vessel damage induced by doxorubicin. Importantly, the researchers explored a promising solution: senolytic treatments. These are special therapies designed to selectively clear out these “zombie” senescent cells.
The findings show that by removing these troublesome senescent cells, the blood vessel dysfunction caused by the chemotherapy can be prevented. This protective effect appears to be linked to better availability of nitric oxide, a molecule vital for blood vessel relaxation, and a reduction in mitochondrial oxidative stress, which is damage to the cell’s energy-producing components. This discovery opens a potential new avenue for protecting patients’ hearts and blood vessels during vital cancer treatments.
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