ReviewMedComm2026
Posttranslational Modifications of p62/SQSTM1 in Health and Disease.
Review in MedComm, 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p62/SQSTM1 is a multifunctional adaptor protein that serves as a central hub integrating cellular stress responses, including selective autophagy, antioxidant defense, metabolism, and immune signaling. Its diverse functions are precisely orchestrated by a complex network of posttranslational modifications (PTMs) that dynamically regulate its conformation, protein interactions, stability, and subcellular localization. This review provides a comprehensive overview of the p62 PTMs landscape, encompassing phosphorylation, ubiquitination, acetylation, methylation, and emerging cysteine-based modifications. We first discuss how these PTMs coordinately maintain cellular homeostasis by fine-tuning autophagic flux, activating antioxidant programs, coordinating nutrient sensing, preserving genomic stability, and regulating immune responses. We then examine how dysregulation of this PTMs network drives pathogenesis in major diseases including cancer, neurodegenerative disorders, metabolic diseases, and infections, with emphasis on context-dependent molecular mechanisms. Furthermore, we summarize current preclinical evidence targeting p62 PTMs. Finally, we emphasize the critical need for advanced technologies to decipher PTMs crosstalk and dynamic regulation, coupled with the development of corresponding therapeutic strategies, to advance precision medicine. Understanding the p62 PTMs code offers promising opportunities for developing novel biomarkers and targeted therapies for human diseases.
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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.