ArticleNature communications2023
Hypoxia-reprogramed megamitochondrion contacts and engulfs lysosome to mediate mitochondrial self-digestion.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 83 citations in OpenAlex.
- Hypoxic conditioning in Parkinson's disease: randomized controlled multiple N-of-1 trials.Nature communications · 2025Trial
- A label-free supramolecular nanoassembly triggers multi-organelle crosstalk-dependent metastasis inhibition via nuclear ROS-HDAC2 axis.Materials today. Bio · 2026Article
- Inhibition of PINK1/Parkin-mediated mitophagy enhances the susceptibility of breast cancer to cuproptosis.Oncogene · 2026Article
- Discovery of organelle-targeted active ingredients combination from Qifu decoction to treat heart failure via modulating cardiac mitochondria-lysosome dysfunction and contacts.Journal of pharmaceutical analysis · 2026Article
- Mitochondrial-derived vesicles drive budding-type fission of damaged lysosomes.Nature cell biology · 2026Article
- Crosstalk collapse: mitochondria-centric organelle network disruption in ovarian aging.Cell communication and signaling : CCS · 2026Review
- Hypoxia-preconditioned mitochondrial transplantation multidirectionally modulates Schwann cell functions to repair peripheral nerve injury in rats.Journal of orthopaedic translation · 2026Article
- AMPK orchestrates mitochondrial homeostasis via dynamics and mitophagy to combat hypoxia-induced energetic crisis in keratocytes.Cell biology and toxicology · 2026Article
- Trifloxystrobin-triggered Drp1 hyperactivation biases mitophagy and imposes long-lasting SVCV susceptibility in teleost.Journal of virology · 2026Article
- Dynamic collaboration between mitochondria and organelles: mechanisms, functions, and disease implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Mitochondria-Derived Vesicles and Mitochondrial Extracellular Vesicles in Health and Cardiovascular Disease.Circulation research · 2026Review
- VAMP4/STX8 Mediate the Autophagic Secretion of Mitochondria and Promote TAMs Polarization in HNSCC.Journal of extracellular vesicles · 2026Article
- PRELID1 and VDAC3 Coordinate a Senescence-Like State in Germinal Center B Cells to Promote IL-7-Driven Antitumor Immunity in Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mitochondrial interplay with membrane organelles in health and disease.Cell communication and signaling : CCS · 2026Review
- The role of mitochondria-associated membranes in tumorigenesis.Discover oncology · 2026Review
- Smart Nanoparticles Disrupting Energy Supply through Triple Mechanisms to Kill Tumors via Dual Disruption of Mitochondria and Lysosomes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting mitochondrial homeostasis as a cancer treatment strategy: current status and future prospects.Molecular cancer · 2026Review
- Cell-free mitochondrial DNA as a potential predictor for hypoxic stress.Molecular biology reports · 2026Article
- Microautophagy: definition, classification, and the complexity of the underlying mechanisms.Autophagy · 2026Review
- Hypoxia-driven tumor immune escape: mechanisms and therapeutic opportunities.Frontiers in immunology · 2026Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are the key organelles for sensing oxygen, which is consumed by oxidative phosphorylation to generate ATP. Lysosomes contain hydrolytic enzymes that degrade misfolded proteins and damaged organelles to maintain cellular homeostasis. Mitochondria physically and functionally interact with lysosomes to regulate cellular metabolism. However, the mode and biological functions of mitochondria-lysosome communication remain largely unknown. Here, we show that hypoxia remodels normal tubular mitochondria into megamitochondria by inducing broad inter-mitochondria contacts and subsequent fusion. Importantly, under hypoxia, mitochondria-lysosome contacts are promoted, and certain lysosomes are engulfed by megamitochondria, in a process we term megamitochondria engulfing lysosome (MMEL). Both megamitochondria and mature lysosomes are required for MMEL. Moreover, the STX17-SNAP29-VAMP7 complex contributes to mitochondria-lysosome contacts and MMEL under hypoxia. Intriguingly, MMEL mediates a mode of mitochondrial degradation, which we termed mitochondrial self-digestion (MSD). Moreover, MSD increases mitochondrial ROS production. Our results reveal a mode of crosstalk between mitochondria and lysosomes and uncover an additional pathway for mitochondrial degradation.
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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.