ReviewCurrent biology : CB2018
Mitophagy and Quality Control Mechanisms in Mitochondrial Maintenance.
Review in Current biology : CB, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,244 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
1,244 citing papers in PubMed.
- Miro1 mediates skeletal muscle insulin resistance in type 2 diabetes.Nature communications · 2026Trial
- The gut microbiome and mitochondrial function in metabolism, immunity, and disease.Gut microbes · 2026Review
- The role and mechanism of UPRmt in adipocytes.Adipocyte · 2026Review
- Revisiting Inherited Metabolic Diseases (IMDs) Through the Lens of Selective Autophagy.Journal of inherited metabolic disease · 2026Review
- β-Asarone Alleviates Post-stroke Neuroinflammation and Improves Mitochondrial Quality Via the BNIP3/BNIP3L-dependent Mitophagy Pathway.Molecular neurobiology · 2026Article
- Failure of Neuroinflammatory Resolution in Brain Aging: Molecular Mechanisms and an Integrative Framework of Microglial Inflammometabolic Locking.Molecular neurobiology · 2026Review
- Article
- Targeting ubiquitin-dependent mitochondrial autophagy and apoptosis in sarcopenia: the therapeutic potential of phytochemicals.Discover nano · 2026Review
- PINK1-mediated mitophagy supports lung cancer initiation and limits the efficacy ofScience advances · 2026Article
- CHCHD2 mitigates age-associated proteostatic collapse by maintaining homeostasis of the mitochondria-lysosome axis.Acta neuropathologica · 2026Article
- Bee-Derived Products in Neurodegenerative Diseases: Bioactive Constituents, Redox-Modulating Mechanisms, Evidence, and Translational Perspectives.Molecules (Basel, Switzerland) · 2026Review
- Article
- Astaxanthin-metformin conjugate nanomicelles-loaded hydrogel reprograms macrophage metabolismBioactive materials · 2026Article
- Mitochondrial dysfunction‑driven ferroptosis in cerebral ischemia‑reperfusion injury: Mechanisms and therapeutic strategies (Review).Molecular medicine reports · 2026Review
- RIPC Protects Against Renal Ischaemia-Reperfusion Injury by Activating SIRT3/Parkin-Mediated Mitophagy.Journal of cellular and molecular medicine · 2026Article
- Article
- Cardiovascular-kidney-metabolic syndrome as a mitochondrial systems disorder.Nature reviews. Nephrology · 2026Review
- Rethinking Drug Resistance in Acute Promyelocytic Leukemia: The Regulated Cell Death Network as an Integrative Framework.Biomolecules · 2026Review
- Disturbances of Mitochondrial Functions and Oxidative Stress Induction in Methylmalonic and Propionic Acidemias: A Critical Role for Metabolite Accumulation.International journal of molecular sciences · 2026Review
- Drugging small-molecule compounds in autophagy-dependent cell death to overcome cancer therapy resistance.Apoptosis : an international journal on programmed cell death · 2026Review
1,184 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
3 authors.
Funding
Abstract
The maintenance of a healthy and functional mitochondrial network is critical during development as well as throughout life in the response to physiological adaptations and stress conditions. Owing to their role in energy production, mitochondria are exposed to high levels of reactive oxygen species, making them particularly vulnerable to mitochondrial DNA mutations and protein misfolding. Given that mitochondria are formed from proteins encoded by both nuclear and mitochondrial genomes, an additional layer of complexity is inherent in the coordination of protein synthesis and the mitochondrial import of nuclear-encoded proteins. For these reasons, mitochondria have evolved multiple systems of quality control to ensure that the requisite number of functional mitochondria are present to meet the demands of the cell. These pathways work to eliminate damaged mitochondrial proteins or parts of the mitochondrial network by mitophagy and renew components by adding protein and lipids through biogenesis, collectively resulting in mitochondrial turnover. Mitochondrial quality control mechanisms are multi-tiered, operating at the protein, organelle and cell levels. Herein, we discuss mitophagy in different physiological contexts and then relate it to other quality control pathways, including the unfolded protein response, shedding of vesicles, proteolysis, and degradation by the ubiquitin-proteasome system. Understanding how these pathways contribute to the maintenance of mitochondrial homeostasis could provide insights into the development of targeted treatments when these systems fail in disease.
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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.