ArticleScientific reports2026
Mechanisms of autophagy-mediated ferroptosis regulation in intestinal mucosal injury under high-G environments.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
High-G (+GZ) exposure is known to induce significant gastrointestinal injury in aviators, yet the underlying mechanisms remain unclear. Ferroptosis is a form of iron-dependent cell death that has been implicated in various pathological conditions, while autophagy plays a critical role in cellular homeostasis and damage regulation. This study investigated the role of autophagy in +Gz-induced intestinal mucosal injury and its interaction with ferroptosis. Sixty female Sprague-Dawley rats were randomly assigned to six groups: control (sham exposure), autophagy inhibition (3-methyladenine, 3-MA), autophagy activation (rapamycin, RAP), +Gz exposure, +Gz exposure with autophagy inhibition, and +Gz exposure with autophagy activation. +Gz exposure was simulated using a small animal centrifuge (+ 10 Gz, 5 min/day for 5 days). Histopathological changes were assessed via haematoxylin-eosin (HE) staining, transmission electron microscopy (TEM), and Chiu scoring. Ferroptosis- and autophagy-related markers (FTH1, NCOA4, GPX4, Nrf2, LC3, and BECN1) were analyzed by Western blotting, quantitative reverse transcription polymerase chain reaction (qRT-PCR), and immunohistochemistry. Levels of Fe
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