Sometimes the most profound medical breakthroughs emerge not from grand theoretical leaps, but from the patient, methodical pursuit of understanding life's most fundamental processes.
Great article. But the peptides, the supplements, the NIR light, the strategies: of what consequence when we know that nanoplastics are lodged in mitochondrial cardiolipin layer, in the oxidative phosphorylation process, these plastics are absorbed by endocytosis into mitochondria. They do not conduct electricity. It seems to me that we have to work on detoxing the body from plastics before the full effect of the healing of dysfunctional mitochondria, which I believe is far more common than we know, this for me is an important step and why I continue the research
Phenomenal breakdown of the cardiolipin-protein complex stabilization. The 2020 PNAS cross-linking data showing SS-31's direct protein interactions is underappreciated, most ppl still think its just an antioxidant when really its acting as a molecular bridge at cardiolipin binding sites. I remember analyzing respiratory complex assembly data back in 2021 and the improvemnts in supercomplex formation were wild, way beyond what you'd expect from simple ROS reduction. One aspect that facinates me is the dose-response in Barth syndrome patients, why do benefits keep accruing past 100 weeks when cardiolipin stability should plateau earlier?
This is a really compelling overview, especially because it focuses on mitochondrial structure/function rather than vague “antioxidant” claims. Clinically, SS-31 / elamipretide is interesting precisely because it targets cardiolipin-rich inner mitochondrial membranes, helping stabilize electron transport and reduce maladaptive oxidative signaling at the source, not just mop up ROS downstream. 
What I appreciate most is the translational framing: mitochondrial dysfunction shows up across heart, skeletal muscle, neurodegeneration, and aging-related syndromes, and cardiolipin biology is a plausible leverage point for improving cellular energetics and resilience. 
At the same time, it’s important to keep the clinical bar clear: while early human studies in mitochondrial disease populations have reported signals like improved exercise performance, SS-31 remains an investigational therapeutic, so dosing, long-term safety, and “who benefits most” still require rigorous trials.
Great article. But the peptides, the supplements, the NIR light, the strategies: of what consequence when we know that nanoplastics are lodged in mitochondrial cardiolipin layer, in the oxidative phosphorylation process, these plastics are absorbed by endocytosis into mitochondria. They do not conduct electricity. It seems to me that we have to work on detoxing the body from plastics before the full effect of the healing of dysfunctional mitochondria, which I believe is far more common than we know, this for me is an important step and why I continue the research
Phenomenal breakdown of the cardiolipin-protein complex stabilization. The 2020 PNAS cross-linking data showing SS-31's direct protein interactions is underappreciated, most ppl still think its just an antioxidant when really its acting as a molecular bridge at cardiolipin binding sites. I remember analyzing respiratory complex assembly data back in 2021 and the improvemnts in supercomplex formation were wild, way beyond what you'd expect from simple ROS reduction. One aspect that facinates me is the dose-response in Barth syndrome patients, why do benefits keep accruing past 100 weeks when cardiolipin stability should plateau earlier?
This is a really compelling overview, especially because it focuses on mitochondrial structure/function rather than vague “antioxidant” claims. Clinically, SS-31 / elamipretide is interesting precisely because it targets cardiolipin-rich inner mitochondrial membranes, helping stabilize electron transport and reduce maladaptive oxidative signaling at the source, not just mop up ROS downstream. 
What I appreciate most is the translational framing: mitochondrial dysfunction shows up across heart, skeletal muscle, neurodegeneration, and aging-related syndromes, and cardiolipin biology is a plausible leverage point for improving cellular energetics and resilience. 
At the same time, it’s important to keep the clinical bar clear: while early human studies in mitochondrial disease populations have reported signals like improved exercise performance, SS-31 remains an investigational therapeutic, so dosing, long-term safety, and “who benefits most” still require rigorous trials.