ReviewInternational journal of molecular sciences2021
Mitophagy in Human Diseases.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
130 citing papers in PubMed, 210 citations in OpenAlex.
- MEN1/menin deficiency suppresses hepatocellular carcinogenesis via disrupting mitophagy-mediated mitochondrial homeostasis.Autophagy · 2026Article
- Rab1A Promotes Hepatic Steatosis by Suppressing Mitophagy via the Raf-1/ERK1/2/PINK1 Signaling Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- The role of phospho-ubiquitin in mitochondrial health and diseases.The Journal of biological chemistry · 2026Review
- Pyrroloquinoline Quinone Mitigates Type 2 Diabetes-Induced Cardiac Injury Through Mitochondrial Quality Control and Inhibition of NLRP3-Dependent Pyroptosis.Metabolites · 2026Article
- A new perspective on mesenchymal stem cells and their derivatives in alleviating cerebral ischemia-reperfusion injury dynamically regulating mitochondrial function to remodel the immune network.Cell death & disease · 2026Review
- FAM162A Is a Key Regulator of Mitochondrial Structure, Dynamics, and Bioenergetics, Driving Cellular Protection and Longevity.Aging cell · 2026Article
- Mitochondria-Targeted Au@Carbon Dot Nanoprobes for SERS Analysis of Drug-Induced Mitophagy.Chemical & biomedical imaging · 2026Article
- Oxidative stress as a converging mechanism of aging and neurodegeneration: From molecular pathways to therapeutic targets.Narra J · 2026Review
- Canonical pathways and selective mechanisms of autophagy in inflammatory bowel disease.Advanced biotechnology · 2026Review
- Immune-metabolic positive feedback model in COPD: cross-mechanisms and potential intervention strategies.Frontiers in cell and developmental biology · 2026Review
- Advances and Therapeutic Potential of Anthraquinone Compounds in Neurodegenerative Diseases: A Comprehensive Review.Drug design, development and therapy · 2026Review
- Investigating the Antidepressant Mechanism of Acupuncture with a Focus on Mitochondrial Homeostasis.International journal of general medicine · 2026Review
- Mitochondrial metabolic reprogramming, quality control, and intercellular transfer in regulating macrophage plasticity.Frontiers in physiology · 2026Review
- Identification and Validation of Mitophagy-Related Biomarkers in Colorectal Cancer: An Integrated Analysis of Single-Cell Transcriptome and Mendelian Randomization.Genetics research · 2026Article
- Cellular stress, cell death, and extracellular vesicles: redefining the therapeutic landscape of rheumatoid arthritis.Clinical rheumatology · 2026Review
- The lysosomal catabolism of nucleic acids-critical regulators of the innate immune system.Nucleic acids research · 2025Review
- Mitophagy as a pivotal axis in non‑alcoholic fatty liver disease: From pathogenic mechanisms to therapeutic strategies (Review).Molecular medicine reports · 2025Review
- Yoda1/Piezo1 Alleviates Lipopolysaccharide-Induced Cardiac Injury via AMPK-Mediated Mitophagy.Cardiovascular toxicology · 2025Article
- The Role of Mitochondrial Dysfunction and Dynamics in Hypertensive Heart Disease: Mechanisms and Recent Advances.Biology · 2025Review
70 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Mitophagy is a selective autophagic process, essential for cellular homeostasis, that eliminates dysfunctional mitochondria. Activated by inner membrane depolarization, it plays an important role during development and is fundamental in highly differentiated post-mitotic cells that are highly dependent on aerobic metabolism, such as neurons, muscle cells, and hepatocytes. Both defective and excessive mitophagy have been proposed to contribute to age-related neurodegenerative diseases, such as Parkinson's and Alzheimer's diseases, metabolic diseases, vascular complications of diabetes, myocardial injury, muscle dystrophy, and liver disease, among others. Pharmacological or dietary interventions that restore mitophagy homeostasis and facilitate the elimination of irreversibly damaged mitochondria, thus, could serve as potential therapies in several chronic diseases. However, despite extraordinary advances in this field, mainly derived from in vitro and preclinical animal models, human applications based on the regulation of mitochondrial quality in patients have not yet been approved. In this review, we summarize the key selective mitochondrial autophagy pathways and their role in prevalent chronic human diseases and highlight the potential use of specific interventions.
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What OpenQuestion holds
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 OpenQuestion graph.