ArticleDevelopmental cell2021
Mitochondrial-derived vesicles compensate for loss of LC3-mediated mitophagy.
Article in Developmental cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 2 of them syntheses that pooled it.
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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.
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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.
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Who cites it
100 citing papers in PubMed, 2 syntheses or guidelines pooled it, 136 citations in OpenAlex.
- The Role of Estrogen in Mitochondrial Disease.Cellular and molecular neurobiology · 2025Pooled it
- Emerging roles of ATG7 in human health and disease.EMBO molecular medicine · 2021Pooled it
- Mitochondrial quality control in health and disease: Updates 2026.Chinese medical journal · 2026Review
- Mitochondrial homeostasis imbalance-triggered PANoptosis in traumatic brain and spinal cord injury: from mechanism to therapeutic strategies.Redox biology · 2026Review
- Review
- Roles of autophagy in brain homeostasis and disease.Nature neuroscience · 2026Review
- Spatial architecture of immunometabolism: Mitochondrial‑organelle interfaces in immune signaling (Review).International journal of molecular medicine · 2026Review
- Cardiac extracellular vesicle proteomics identifies mitochondrial and contractile dysfunction in carbon monoxide poisoning and their reversal by hyperbaric oxygen therapy.Molecular medicine (Cambridge, Mass.) · 2026Article
- Mitochondrial homeostasis: the central hub governing the progression of atherosclerosis.Precision clinical medicine · 2026Review
- Extracellular vesicles from IPFP-MSCs trigger osteoarthritis by transferring mtDNA.Bioactive materials · 2026Article
- Rapid optogenetic manipulation of autophagy reveals that the nuclear pore complex is a robust autophagy substrate.bioRxiv : the preprint server for biology · 2026Article
- Microautophagy: current understanding of its molecular mechanisms and functions.Autophagy reports · 2026Review
- Novel therapeutic strategies targeting mitochondrial quality control for metabolic dysfunction-associated steatotic liver disease.Frontiers in physiology · 2026Review
- Integrating the hallmarks of cancer into autophagy: a perspective from underlying mechanisms to therapeutic strategies.Theranostics · 2026Review
- Mitophagy in the pathogenesis and management of disease.Cell research · 2026Review
- Mitochondrial dysfunction and PANoptosis-related signaling in acute central nervous system injuries: mechanistic convergence and therapeutic opportunities.Frontiers in molecular neuroscience · 2026Review
- Mitochondria-derived vesicles serve as reactors in response to stress in cardiomyocytes.Cell communication and signaling : CCS · 2025Article
- Mechanism of autophagy initiation by transmembrane selective autophagy receptors.The EMBO journal · 2025Review
- From Mitochondria to Immunity: The Emerging Roles of Mitochondria-Derived Vesicles and Small Extracellular Vesicles in Cellular Communication and Disease.Journal of extracellular vesicles · 2025Review
- Sensing within: Mitochondrial inside-out signal transduction.Cell chemical biology · 2025Review
40 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria are critical metabolic and signaling hubs, and dysregulated mitochondrial homeostasis is implicated in many diseases. Degradation of damaged mitochondria by selective GABARAP/LC3-dependent macro-autophagy (mitophagy) is critical for maintaining mitochondrial homeostasis. To identify alternate forms of mitochondrial quality control that functionally compensate if mitophagy is inactive, we selected for autophagy-dependent cancer cells that survived loss of LC3-dependent autophagosome formation caused by inactivation of ATG7 or RB1CC1/FIP200. We discovered rare surviving autophagy-deficient clones that adapted to maintain mitochondrial homeostasis after gene inactivation and identified two enhanced mechanisms affecting mitochondria including mitochondrial dynamics and mitochondrial-derived vesicles (MDVs). To further understand these mechanisms, we quantified MDVs via flow cytometry and confirmed an SNX9-mediated mechanism necessary for flux of MDVs to lysosomes. We show that the autophagy-dependent cells acquire unique dependencies on these processes, indicating that these alternate forms of mitochondrial homeostasis compensate for loss of autophagy to maintain mitochondrial health.
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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 OpenQuestion graph.