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Author Spotlight: Decoding Mitochondrial Aging
Published on: June 30, 2023
Mitochondrial Dysfunction in Aging, HIV, and Long COVID: Mechanisms and Therapeutic Opportunities
María Victoria Delpino1, Jorge Quarleri1
1Laboratorio de Inmunopatología Viral, Instituto de Investigaciones Biomédicas en Retrovirus y Sida (INBIRS), Universidad de Buenos Aires, Consejo de Investigaciones Científicas y Técnicas (CONICET), Buenos Aires 1121, Argentina.
Abstract:
We hypothesize that a unified mitochondrial perspective on aging, HIV, and long COVID reveals shared pathogenic mechanisms and specific therapeutic vulnerabilities that are overlooked when these conditions are treated independently. Mitochondrial dysfunction is increasingly recognized as a common factor driving aging, HIV, and long COVID. Shared mechanisms-including oxidative stress, impaired mitophagy and dynamics, mtDNA damage, and metabolic reprogramming-contribute to ongoing energy failure and chronic inflammation. Recent advancements highlight new therapeutic strategies such as mitochondrial transfer, transplantation, and genome-level correction of mtDNA variants, with early preclinical and clinical studies providing proof-of-concept. This review summarizes current evidence on mitochondrial changes across aging and post-viral syndromes, examines emerging organelle-based therapies, and discusses key challenges related to safety, durability, and translation.
Insights
A unified mitochondrial view reveals shared aging, HIV, and long COVID mechanisms. Emerging organelle therapies offer new treatment avenues for these interconnected conditions.
Area of Science:
- Mitochondrial biology
- Aging research
- Infectious diseases
- Post-viral syndromes
Background:
- Mitochondrial dysfunction is a common pathway in aging, HIV, and long COVID.
- Independent treatment approaches may overlook shared pathogenic mechanisms.
Purpose of the Study:
- To explore a unified mitochondrial perspective on aging, HIV, and long COVID.
- To identify shared mechanisms and therapeutic vulnerabilities.
- To review emerging organelle-based therapies.
Main Methods:
- Literature review of current evidence on mitochondrial changes.
- Examination of shared mechanisms: oxidative stress, mitophagy, mtDNA damage, metabolic reprogramming.
- Analysis of emerging therapeutic strategies: mitochondrial transfer, transplantation, mtDNA correction.
Main Results:
- Mitochondrial dysfunction drives energy failure and chronic inflammation in aging, HIV, and long COVID.
- Shared mechanisms include oxidative stress, impaired mitophagy, mtDNA damage, and metabolic reprogramming.
- New therapies like mitochondrial transfer show preclinical and clinical proof-of-concept.
Conclusions:
- A unified mitochondrial perspective highlights interconnectedness between aging, HIV, and long COVID.
- Organelle-based therapies present promising, yet challenging, future treatment options.
- Further research is needed on safety, durability, and translation of these novel therapies.
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