Researchers in the field of biology have discovered that senescent cells accumulating in the body can be programmed to self-destruct by inhibiting the GPX4 protein. According to TASS, citing the press service of the UK Medical Research Council (MRC), the elimination of these cells in mice led to a slowing of tumor development. Mariantonietta D’Ambrosio, an MRC research fellow, noted that senescent cells were previously considered therapeutically safe in oncology due to their inability to divide. However, it has now been established that over time, they secrete signaling molecules that stimulate the growth of adjacent malignant formations, which prompted scientists to look for ways to eliminate them. Senescent cells are defined as cells that have stopped dividing due to accumulated damage or telomere shortening. Drugs known as senolytics are being developed to combat cellular senescence. British scientists managed to identify a new class of such compounds. During the screening of 10.4 thousand molecules on cultures of senescent cells, four were discovered that initiated a previously unknown form of apoptosis linked to ferroptosis—cell death due to the accumulation of iron or reactive oxidants. Further research confirmed that these molecules trigger ferroptosis by suppressing the activity of the GPX4 protein, which usually protects cell membranes from oxidative damage. Scientists found that senescent cells are in a state of severe oxidative stress, and without GPX4 protection, they die. Oxidative stress is also a characteristic feature of tumors. Experiments in mice showed that the new senolytics enhance the effectiveness of standard chemotherapy for breast, prostate, and ovarian cancer, increasing the lifespan of the rodents by several weeks.
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