ReviewInternational journal of molecular medicine2026
Autophagy determines the fate of immune cells by regulating metabolic remodeling and PANoptosis (Review).
Review in International journal of molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy, as a core mechanism for maintaining cellular homeostasis, influences differentiation and functional activation of immune cells by regulating metabolic reprogramming. Crucially, autophagy serves as a molecular switch that precisely modulates differentiation and subsequent cell fate decisions. It achieves this by eliminating intracellular danger signals or key complexes, thereby determining whether immune cells undergo PANoptosis, an inflammatory death mode that integrates features of pyroptosis, apoptosis and necroptosis. The present review systematically discusses the regulatory role of autophagy in the developmental, differentiation and metabolic pathways of various immune cells. Furthermore, it elucidates the mechanistic details by which autophagy, and particularly mitophagy, dampens excessive PANoptosis activation through the elimination of danger signals (such as mitochondrial DNA and reactive oxygen species) or the degradation of PANoptosome components. Additionally, it clarifies the molecular mechanism by which autophagy dysregulation, induced by specific pathological conditions, leads to inflammatory responses and immunopathological damage. Overall, this review establishes the significance of the autophagy‑PANoptosis axis in the development and progression of autoimmune diseases and tumors, providing a solid theoretical foundation for the optimization and innovation of therapeutic strategies for these diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.