Mitochondria are organelles found in most cells, better known for generating chemical energy required to supply cellular functions. More and more
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Mitochondria are organelles found in most cells, better known for generating the chemical energy required to feed cellular functions. However, more and more, researchers are discovering how mitochondrial function, and dysfunction play critical roles in numerous diseases and even aging. In a new study, the online edition of August 4, 2022 of immunity, scientists of the Faculty of Medicine of San Diego of the University of California and the Institute of Biological Studies of Salk report a surprising link between the mitochondria, the inflammation and DNMT3A and TET2, a couple of genes that normally help regulate the growth of blood blood cells, but when it is mutated, they are associated with a greater risk of atherosclerosis. “We find that DNMT3A and TET2 genes, in addition to their normal work to alter chemical labels to regulate DNA, directly activate the expression of a gene involved in the mitochondrial inflammatory pathways, which suggests as a new molecular objective for therapeutic atherosclerosis” Said Gerald Gerald Shadel, PHD, co-senior study author and director of the San Diego Nathan Shock Excellence in the basic biology of aging at the Salk Institute. “They also interact with mitochondrial inflammatory pathways, which hint a new molecular objective for atherosclerosis therapy.” While studying the roles of the DNMT3A and Tet2 mutations in clonal hematopoiesis, which occurs when stem cells begin to make new blood cells with the same genetic mutation, author of Co-Senior study Christopher Glass, MD, PHD, teacher in the departments of medicine and cellular and cellular and cellular molecular medicine in the School of Medicine of the UC San Diego, and its colleagues indicated that the abnormal inflammatory signage related to the deficiency of DNMT3A and Tet2 in the blood cells played an important role in the Inflammation response that promotes the development of atherosclerosis. But the question was still how DNMT3a and TET2 genes were involved in inflammation and atherosclerosis: the accumulation of fatty plates in the arteries and the main cause of cardiovascular disease. It is estimated that approximately half of the Americans between the ages of 45 and 84 have atherosclerosis, which is the main cause of the United States and westernized nations. “The problem was that we could not solve how DNMT3A and TET2 were involved because the proteins that apparently codify opposite things regarding DNA regulation,” Glass said. “His antagonistic activity led us to believe that there may be other mechanisms at stake, which led us to adopt a different approach and
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