ReviewFrontiers in endocrinology2026
Endoplasmic reticulum stress in skeletal muscle dysfunction of type 2 diabetes: mechanisms and therapeutic implications.
Review in Frontiers in endocrinology, 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
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
1 citing paper in PubMed.
- Stigmasterol ameliorates obesity-associated insulin resistance by activating the PPARγ pathway and alleviating oxidative stress.Frontiers in endocrinology · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
With the continuous rise in the global prevalence of type II diabetes mellitus (T2DM), the associated skeletal muscle complications, including insulin resistance, muscle atrophy, and physical frailty, have garnered increasing attention. Skeletal muscle plays a vital role as a metabolic and endocrine organ and is considered a key factor in the pathological mechanisms of T2DM. Despite significant advances in understanding, the intrinsic molecular mechanisms underlying skeletal muscle dysfunction remain incompletely elucidated. Recent studies have highlighted a significant cellular stress response known as endoplasmic reticulum stress (ERS), which is triggered by hyperglycemia, lipotoxicity, and inflammation, and may serve as a pivotal hub in T2DM pathology. This review narratively examines published articles from the past five years, focusing on experimental studies related to ERS and T2DM myopathy. Comprehensive searches were conducted in electronic databases for journal articles published between 2020 and 2025.This review synthesizes experimental studies to elucidate how ERS disrupts muscle homeostasis via the unfolded protein response (UPR) pathways (PERK, IRE1α, and ATF6) contributing to insulin resistance and activation of protein degradation systems. Consequently, intervention strategies targeting ERS may offer new insights and directions for the prevention and treatment of T2DM-related muscle disorders. This review aims to explore the mechanisms by which ERS contributes to T2DM myopathy, identifying potential therapeutic targets and providing a foundation for future clinical research.
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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.