ArticleiScience2026
Lipid overload triggers PERK-ALCAT1-mediated mitophagy failure in hepatocytes.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Calcium imbalance drives organelle network collapse and immune remodeling: novel pathogenic mechanisms in MASLD progression.Frontiers in immunology · 2026Review
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria-associated endoplasmic reticulum membranes (MAMs), contact sites between the endoplasmic reticulum (ER) and mitochondria, are critical for calcium signaling and lipid metabolism. However, how MAMs contribute to mitochondrial dysfunction in lipid overload-induced fatty liver remains unclear. Here, using teleost fish as a model, we showed that high-fat diets promoted the aggregation of PERK and ALCAT1 at MAMs, causing mitochondrial calcium overload and membrane depolarization, and impairing PINK1/Parkin-dependent mitophagy. Acetylation of PERK at lysine 388 facilitated its binding to ALCAT1, while activation of SIRT1 by resveratrol induced site-specific deacetylation of PERK, disrupted PERK-ALCAT1 interaction, and restored mitophagy and mitochondrial integrity. These findings revealed a conserved SIRT1-PERK-ALCAT1 signaling axis linking ER stress to mitophagy failure and identified a potential nutritional intervention to alleviate lipid-induced hepatic injury. This mechanism is conserved across species and offers a basis for controlling metabolic dysfunction-associated steatotic liver disease (MASLD) in teleosts and potentially other vertebrate systems.
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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 Socratic graph.