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How mitochondria drives senescence, affecting healthy ageing


Key points from article :

Mitochondria (mt) trigger senescence through communication with the cell's nucleus.

Experiments using human lung cell model of senescence.

Found out mt drives formation of pro-inflammatory cytoplastic chromatin.

HDAC inhibitor, an FDA-approved drug, transformed senescent cells.

From a large and flat form to a healthier and more visually youthful condition.

Resulting cells had better mt function, less cytoplasmic chromatin and inflammatory signals.

Observed same benefits in mice livers where senescence was induced.

Search is on for less toxic senescence-inhibiting drugs.

Like a compound that interrupts the communication between the mitochondria and the nucleus.

This study provides the first concrete link between known hallmarks of aging.

Research by Sanford Burnham Prebys Medical Discovery Institute, Harvard University scientists.

Published in Genes & Development.

Potential target for drug-based interventions to delay cellular ageing identified

Mentioned in this article:

Click on resource name for more details.

Genes & Development

Publishes research in molecular biology, genetics, cancer biology, biochemistry

Glenn Foundation For Medical Research

The mission of the Glenn Foundation For Medical Research is to extend the healthy years of life

Harvard University

Private Ivy League research university in Massachusetts

Mark R Collins

President of Glenn Foundation for Medical Research

Peter D. Adams

Co-Director Aging, Cancer and Immuno-oncology at SBP, Co-Editor-in-Chief Aging Cell

Sanford Burnham Prebys Medical Discovery Institute

Conducts collaborative research to find new therapies and improve quality of life