ReviewCells2026
Skeletal Muscle Insulin Resistance in Three Dimensions: Mechanisms, Myokines, and Microphysiological Platform.
Review in Cells, 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
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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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Skeletal muscle insulin resistance is a major determinant of impaired glucose disposal in type 2 diabetes. The mechanisms underlying insulin resistance in muscles are shaped by tissue architecture, contraction, extracellular-matrix signalling, mitochondrial function, and endocrine communication; processes that are not fully reproduced by conventional cell-based two-dimensional (monolayer) models of disease. This narrative review integrates our current understanding of canonical IRS-1-PI3K-AKT-GLUT4 signalling with contraction-dependent pathways, lipotoxicity, mitochondrial and endoplasmic-reticulum stress, inflammation, extracellular-matrix remodelling, and myokine dysregulation. We then evaluate experimental models, with particular emphasis on three-dimensional (3D) engineered muscle tissues (EMTs). Current evidence indicates that 3D EMTs can provide aligned myofibres, matrix-dependent mechanosignalling, measurable force and calcium handling, insulin-stimulated glucose uptake, and contraction-regulated myokine secretion. Emerging co-culture and myosteatosis models also recapitulate aspects of adipose-muscle crosstalk. However, current platforms remain limited by incomplete fibre maturation, absent or immature neuromuscular junctions, limited vascularisation and perfusion, variability across cell and scaffold systems, and sparse validation against patient-specific multi-omic signatures. Integrating patient-derived cells, innervation, perfusion, controlled mechanics, and multi-tissue modules could make 3D EMTs a more predictive microphysiological platform for mechanistic studies, therapeutic screening, and precision metabolic medicine.
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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 OpenQuestion graph.