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LEAF interviews Alexander Fedintsev about weak v strong ECM hypothesis

It may be a new hallmark of ageing, but it's been one of SENS' 7 strategies since it started

15-Jul-2020

Key points from article :

Research into damage accumulation in long-living macromolecules published in Ageing Research Reviews.

Idea that non-enzymatic extracellular matrix cross-links are primary cause of aging was proposed by Björksten in 1942.

Damage of cross-linking is not mentioned in The Hallmarks of Aging.

Weak ECM hypothesis = damage to long-lived macromolecules is just one of the drivers of aging.

Strong ECM hypothesis = cellular aging is caused mainly by ECM degeneration.

Cells are rejuvenated when transferred into young ECM.

ECM is causatively linked to cellular senescence.

The anti-fibrotic nature of cellular senescence has been demonstrated in multiple studies.

Glycated, aging ECM may be indistinguishable from fibrotic ECM.

We could reverse age-related pathologies solely by targeting the ECM degradation.

Mice/rats are unsuitable for testing potential drugs since their ECM cross-links have a methylglyoxal origin.

Enzyme that breaks glucosepane cross-links probably unable to fit between collagen fibrils.

Mentioned in this article:

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Ageing Research Reviews

Scientific journal covering ageing published by Elsevier

Alexander Fedintsev

Scientist, bioinformatician and machine learning engineer

Topics mentioned on this page:
Ageing Research, Senescent Cells