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An investigation led by Vall d’Hebron Research Institute (Vhir) of Barcelona has identified in animal models a mechanism for which he heart aging favors the heart failureone of the main causes of disability, rehospitalization and death in older people.
The work, in collaboration with the areas of Cardiovascular Diseases and Epidemiology and Public Health of the CIBER, he National Center for Cardiovascular Research (CNIC) and the Thomas Jefferson University of Philadelphia, and published in the magazine Aging Cell, has described a “key cause” which favors the deterioration of the heart with aging, Vhir reported this Tuesday in a statement, according to Europa Press.
The team has studied animal models that they achieve physiologically advanced agescombined with cell models aging simulation.
Through high resolution microscopy techniques and massive proteomic analysishave been analyzed in detail internal changes of cells.
Researchers have identified the “key role” of the advanced glycation products (AGEs) about the mitochondriathe organelles responsible for generating energy inside the cells.
The AGE are chemical compounds derived from metabolism and, as they accumulate in the mitochondria, they make these organelles lose energy efficiency. This process triggers a chain effect: he chemical damage also affects the lysosomesresponsible for eliminating damaged cellular components, and causes a progressive alteration of the cellular recycling systemfavoring the accumulation of waste inside cells.
The persistence of this cellular stress makes a part of the cardiomycytes enter a state of senescencea transformation that allows them survivebut affects your normal function.
“These cells, although they do not die, develop important structural and functional changes and adopt a pro-inflammatory profile that spreads locally and contributes to the deterioration of the heart,” explained lead researcher Marisol Ruiz-Meana.
New therapeutic avenues
The results open the door to new strategies for prevent or delay heart failure associated with aging. In particular, intervene on the mechanisms that generate AGE either restore the digestive activity of lysosomes could be promising therapeutic avenues.
Ruiz-Meana has stressed that the identification of this mechanism “allows us to better understand how the aging favors the onset of heart failure and open new opportunities to develop therapies aimed at protecting the heart“.
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