An international team of researchers has uncovered a previously unknown molecular mechanism linking mitochondrial function, cellular metabolism, and chronic age-related inflammation. According to a study published in the journal Nature, these processes can be blocked to preserve health in old age, infohub.kz reports.
The work involved specialists from the Sanford Burnham Prebys Medical Discovery Institute, Mayo Clinic, and affiliated institutions. According to ScienceDaily, experiments demonstrated that the drug CTPI-2 blocks signals from 'zombie cells' and extends healthy longevity.
With age, so-called senescent cells, or 'zombie cells,' accumulate in tissues. They stop dividing but continue to release inflammatory molecules—the SASP phenotype. The authors, led by Peter Adams and João Passos, found that this process is triggered by the intersection of two mitochondrial pathways.
First, mitochondria in senescent cells produce increased amounts of acetyl-CoA, which unwinds histones and opens access to inflammatory genes. Second, damaged mitochondria release DNA and RNA, providing an immune signal to activate these exposed genes.
Scientists tested CTPI-2 in mice; the drug blocks a transporter protein required for acetyl-CoA synthesis. Blocking the metabolic signal made inflammatory genes inaccessible, significantly reducing systemic inflammation and improving tissue function in aging animals.
According to the authors, the use of inhibitors like CTPI-2 opens a new therapeutic direction in combating age-related decline.