ReviewFrontiers in immunology2026
Research progress on tumor extracellular matrix stiffness and immunosuppression.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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Who cites it
2 citing papers in PubMed.
- FAK Mediated Coordination of Extracellular Matrix Remodeling and Cellular Mechanics Impairs Nanomedicine Delivery in Solid Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A review of soluble mediator and cytokine networks linking combination immunotherapy, tumor microenvironment remodeling and skeletal muscle dysfunction.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor matrix stiffness, a pivotal physical attribute of the tumor microenvironment, has evolved from a passive physical barrier to an active immunoregulatory platform, profoundly impacting the initiation and effector phases of anti-tumor immune responses. This review systematically elaborates on the dual mechanisms that drive immunosuppression. Directly, stiffness attenuates T-cell and natural killer (NK) cell functions by activating pathways such as Yes-associated protein (YAP)/Transcriptional co-activator with PDZ-binding motif (TAZ) and Piezo-type mechanosensitive ion channel component 1 (Piezo1). It also drives the polarization of macrophages and dendritic cells towards immunosuppressive phenotypes. Indirectly, stiffness fosters an immune escape ecosystem by persistently activating cancer-associated fibroblasts, inducing tumor cell epithelial-mesenchymal transition, and upregulating immune checkpoints. Consequently, strategies such as enzymatic degradation, targeting mechanotransduction pathways, employing anti-fibrotic drugs, and developing intelligent combination therapies have emerged, aiming to soften tumors and reverse immunosuppression. Clinical studies confirm that high expression of the mechanosignaling hub Yes-associated protein 1 (YAP1) is associated with resistance to immunotherapy. In the future, integrating mechanobiology, immunometabolism, and smart materials to develop precise multimodal combination strategies holds promise for reversing the "cold tumor" microenvironment and opening new avenues to overcome immunotherapy resistance in solid tumors.
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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.