ArticleNature communications2025
An unconventional autophagic pathway that inhibits ATP secretion during apoptotic cell death.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The trial behind it
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Who cites it
9 citing papers in PubMed.
- Reprogramming Autophagy to Strengthen Antitumour Immunity: Advances in Immunotherapeutic Strategies.Immunology · 2026Review
- Structural and molecular principles of DAMP biology.Nature structural & molecular biology · 2026Review
- The Marine-Derived Cyclopentapeptide Turnagainolide B Suppresses Melanoma via Autophagic Flux Disruption and Inhibits Tumorigenesis In Vivo.Marine drugs · 2026Article
- Regulation of Innate Immune Signaling by Autophagy.International journal of molecular sciences · 2026Review
- Looking at the fraction with Annexin V⁺ and propidium iodide⁺: insights into cell death types from preclinical studies in solid and haematological cancers.Apoptosis : an international journal on programmed cell death · 2026Review
- Fighting the invader: strategies against intracellular bacteria.Frontiers in pharmacology · 2026Review
- CanPharmaceuticals (Basel, Switzerland) · 2025Review
- Unconventional role of ATG16L1 in the control of ATP compartmentalization during apoptosis.Autophagy · 2025Article
- Inflammation preservation strategy: reconciling pain control and disc resorption in lumbar disc herniation.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Mobilisation of Damage-Associated Molecular Patterns (DAMPs) determines the immunogenic properties of apoptosis, but the mechanisms that control DAMP exposure are still unclear. Here we describe an unconventional autophagic pathway that inhibits the release of ATP, a critical DAMP in immunogenic apoptosis, from dying cells. Mitochondrial BAK activated by BH3-only molecules interacts with prohibitins and stomatin-1 through its latch domain, indicating the existence of an interactome specifically assembled by unfolded BAK. This complex engages the WD40 domain of the autophagic effector ATG16L1 to induce unconventional autophagy, and the resulting LC3-positive vesicles contain ATP. Functional interference with the pathway increases ATP release during cell death, reduces ATP levels remaining in the apoptotic bodies, and improves phagocyte activation. These results reveal that an unconventional component of the autophagic burst that often accompanies apoptosis sequesters intracellular ATP to prevent its release, thus favouring the immunosilent nature of apoptotic cell death.
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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.