Metastudy reviews impact of mitochondrial aging on cardiovascular disease


As we age our mitochondria become increasingly damaged and dysfunctional.
One possible reason is the failure of autophagy and mitophagy.
Autophagy is our cells’ way of removing damaged components, allowing healthy ones to replace them.
Mitophagy occurs when autophagy selectively breaks down worn out or damaged mitochondria.
Particularly affects tissues with high energy requirements, including the heart.
Meta-study finds that enhanced mitophagy preserves cardiac homeostasis and extends life span.
Possible approaches to address the age-related decline of mitophagy include:
- increase energy output of mitochondria by delivering NAD+ precursors to the cells
- delivery of targeted antioxidants (e.g. mitoQ, SkQ) - lab & human trial results somewhat uncertain
- directly repair mitochondria - SENS Research Foundation researching these as part of its MitoSENS programme
Review by University of California, San Diego, published in Frontiers in Cardiovascular Medicine.

Still lots to discover, but SENS already looking at ways to stop it in its tracks

Mentioned in this article:

Resource Frontiers in Cardiovascular Medicine - Journal covering basic, translational, and clinical cardiovascular medicine

Resource SENS Research Foundation

Resource University of California - Public research university with 10 campuses and 5 medical centres

Read full article on Life Extension Advocacy Foundation (LEAF) website
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