ReviewSignal transduction and targeted therapy2025
Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances.
Review in Signal transduction and targeted therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 446 papers.
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Who cites it
446 citing papers in PubMed.
- Artificial intelligence-guided nanozyme engineering for chronic wound healing: from rational design to precision therapeutics.Bioactive materials · 2027Review
- Integrated transcriptome and metabolome revealVirulence · 2026Article
- Bioinspired 0D mitochondrial bioenergetic actuators rewire cartilage progenitor cell metabolism for osteoarthritis remission.Bioactive materials · 2026Article
- Gut‑liver‑kidney axis: A systems biology framework for understanding and treating chronic kidney disease (Review).International journal of molecular medicine · 2026Review
- A biomimetic core-shell nanofibrous dressing for temporally coordinated infection control and mitochondrial protection in diabetic wounds.Materials today. Bio · 2026Article
- Mitochondrial quality control in acute liver injury and its therapeutic implications (Review).Molecular medicine reports · 2026Review
- Advances in DNA nanostructures for pathogenic microorganisms.Materials today. Bio · 2026Review
- Micronutrients and omega-3 PUFAs to promote healthy ageing: informing a physiology-based complementation strategy.GeroScience · 2026Review
- ROS scavenging mitigates TNFα-induced endoplasmic reticulum stress and mitochondrial fragmentation in human airway smooth muscle.Function (Oxford, England) · 2026Article
- Mitochondrial Transplantation Rejuvenates Aging Heart by Restoring Mitophagy Flux via the HIF-3α-BNIP3 Axis.Aging cell · 2026Article
- Lipoic acid synthase modulates psoriasis-like keratinocyte dysfunction in association with oxidative stress, ferroptosis-associated remodeling, and STAT3/NF-κB activation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Evaluation the role of quinoa seeds in attenuation the brain cellular senescence and aging induced by D-galactose and γ-radiation in rats: insights into autophagy, telomerase activity, amyloid-β and tau proteins.Inflammopharmacology · 2026Article
- Limosilactobacillus reuteri orchestrates IAA-mediated mitochondrial homeostasis and stem cell renewal against intestinal oxidative injury in aged hens.Journal of animal science and biotechnology · 2026Article
- Dexpanthenol Attenuates High Fructose Corn Syrup-Induced Brain Injury by Modulating Oxidative Stress, Neuroinflammation, Apoptotic Signaling and Amyloidogenic Gene Expression.Molecular neurobiology · 2026Article
- Closed-Loop Neuromodulation for Brain Fatigue: From Real-Time Biomarkers to Adaptive Intervention.International journal of molecular sciences · 2026Review
- Longitudinal infection trajectories and biological aging acceleration in adults: a prospective cohort study.GeroScience · 2026Article
- The Gut Microbiome as a Mechanistic Link Between the Planetary Health Diet and Healthy Aging.Nutrients · 2026Review
- Defect-Regulated Hetero-Trimetallic Nanocatalysts Augment Sonocatalytic Dynamic Therapy by Charge Transfer Facilitation and Ferroptosis Cascade Induction.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Mitochondria-Targeted Nanotherapies in Aging Neurodegenerative Disorders: Emerging Prospects and Clinical Potential.Advanced healthcare materials · 2026Review
- Network Model to Predict Age-Related Transcriptional Reprogramming.Aging cell · 2026Article
386 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Mitochondria are the energy production centers in cells and have unique genetic information. Due to the irreplaceable function of mitochondria, mitochondrial dysfunction often leads to pathological changes. Mitochondrial dysfunction induces an imbalance between oxidation and antioxidation, mitochondrial DNA (mtDNA) damage, mitochondrial dynamics dysregulation, and changes in mitophagy. It results in oxidative stress due to excessive reactive oxygen species (ROS) generation, which contributes to cell damage and death. Mitochondrial dysfunction can also trigger inflammation through the activation of damage-associated molecular patterns (DAMPs), inflammasomes and inflammatory cells. Besides, mitochondrial alterations in the functional regulation, energy metabolism and genetic stability accompany the aging process, and there has been a lot of evidence suggesting that oxidative stress and inflammation, both of which are associated with mitochondrial dysfunction, are predisposing factors of aging. Therefore, this review hypothesizes that mitochondria serve as central hubs regulating oxidative stress, inflammation, and aging, and their dysfunction contributes to various diseases, including cancers, cardiovascular diseases, neurodegenerative disorders, metabolic diseases, sepsis, ocular pathologies, liver diseases, and autoimmune conditions. Moreover, we outline therapies aimed at various mitochondrial dysfunctions, highlighting their performance in animal models and human trials. Additionally, we focus on the limitations of mitochondrial therapy in clinical applications, and discuss potential future research directions for mitochondrial therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.