Heart disease still kills nearly 20 MILLION people every year worldwide — roughly 1 person every 1.5 seconds. — But what if medicine could move beyond simply slowing plaque buildup…and actually REMOVE toxic oxidized cholesterol from arteries? — Dr. Matthew “Oki” O’Connor, CEO and Co-Founder, Cyclarity Therapeutics.

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In the time it will take you watch this episode, over 2,000 people around the world will die from diseases driven by arterial plaque. But what if we could actually remove the toxic cholesterol already trapped inside arteries?

Today we’re diving into one of the biggest unsolved problems in medicine and aging: how do you actually remove arterial plaque instead of merely slowing its progression?

Cardiovascular disease remains the world’s leading killer, despite decades of statins, anti-inflammatory drugs, and newer RNA-based therapies. Most existing treatments help manage cholesterol and reduce risk, but very few directly target the toxic debris already embedded inside plaques.

But what if we could literally extract some of the most dangerous oxidized cholesterol molecules from the body?

Researchers at Bar-Ilan University have successfully restored youthful patterns of DNA organization in the livers of old mice, reversing key molecular features associated with aging. The study, published in Nature Communications, identifies the protein SIRT6 as a powerful protector against age-related breakdown in chromatin, the complex system that packages DNA and controls how genes are switched on and off.

The findings suggest that aging is not simply a passive process of wear and tear, but may be driven in part by reversible changes in the way DNA is organized inside cells.

DNA inside cells is tightly folded and packaged into chromatin, a structure that acts like a biological control system for gene activity. Using advanced tools to study DNA organization and gene activity, the researchers examined multiple molecular changes in the livers of young and old mice. What they discovered was dramatic: aging disrupts chromatin architecture in the liver, causing inflammatory pathways to become overactive while weakening the metabolic programs that define healthy liver tissue.

Emerging evidence suggests that organs age at different rates. This study identifies a mechanism by which the naturally hypoxic intervertebral disc ages relatively slowly, via selective autophagy of HIF-1α, and designs a small molecule to export this mechanism across tissues.