
Mitophagy: The Cellular Cleanup System That Decides Aging, Heart Disease, and Vision Loss
From The Energy Code by Dr. Mike Belkowski
May 21, 2026 · 56 min · Episode 350
About this episode
This episode discusses the critical role of mitophagy in aging and various diseases, emphasizing the importance of mitochondrial cleanup.
Mitophagy sounds technical — until you realize it may be one of the most important biological processes behind aging, cardiovascular disease, eye degeneration, inflammation, and cellular energy. In this episode, Dr. Mike and Don break down three recent scientific reviews that converge on one central message: when mitochondrial cleanup fails, tissues don’t just lose ATP — they become inflamed, oxidatively stressed, and vulnerable to disease. You’ll learn the difference between autophagy and mitophagy, why damaged mitochondria act like inflammatory “danger beacons,” what this looks like in Fabry disease cardiomyopathy, inflammatory cardiovascular disease, and ophthalmic diseases like glaucoma/AMD/diabetic retinopathy — and why the future of mitochondrial medicine is about restoring the rhythm of removal + renewal. (Educational content only, not medical advice.) - Articles Referenced in Episode: Mitophagy in ophthalmic pathologies: Molecular mechanisms and therapeutic implications Understanding Dysfunctional Autophagy and Mitophagy in Inflammatory Cardiovascular Disease Early mitophagy defects and impaired mitochondrial energy metabolism drive target organ damage progression…
People in this episode
Host: Dr. Mike Belkowski
Guest: Don
Topics covered
- mitophagy
- aging
- cardiovascular disease
- inflammation
- cellular energy
- ophthalmic diseases
Keywords
- mitophagy
- autophagy
- inflammation
- cardiomyopathy
- cellular energy
- disease
- oxidative stress
Mentioned in this episode
Books & works: Mitophagy in ophthalmic pathologies: Molecular mechanisms and therapeutic implications, Understanding Dysfunctional Autophagy and Mitophagy in Inflammatory Cardiovascular Disease, Early mitophagy defects and impaired mitochondrial energy metabolism drive target organ damage progression: lessons from the Fabry heart
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