What does this research mean for the field?

USP7-mediated stabilization of Snail1 via the TGF-β1/Smad3 pathway drives macrophage-to-myofibroblast transition in postoperative peritoneal adhesions, a process that can be therapeutically attenuated by Olaparib. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To determine the cellular origins of myofibroblast accumulation in postoperative peritoneal adhesions and characterize the molecular signaling pathway driving macrophage-to-myofibroblast transition.

September 14, 2026Molecular MedicineOpen Access

USP7-mediated stabilization of Snail1 drives macrophage-to-myofibroblast transition and promotes postoperative peritoneal adhesions

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Authors

LGLi Gan SZSihan Zhao BHBowen Huo

Discussion

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Overview

Preclinical study demonstrates that USP7 stabilizes Snail1 to drive macrophage transition into myofibroblasts, indicating that targeting USP7 alleviates postoperative adhesions.

Key Points

To determine the cellular origins of myofibroblast accumulation in postoperative peritoneal adhesions and characterize the molecular signaling pathway driving macrophage-to-myofibroblast transition.
Established a mouse model of postoperative peritoneal adhesions and used immortalized bone marrow-derived macrophages to model macrophage-to-myofibroblast transition in vitro.
Performed transcriptome sequencing, RNA interference, dual-luciferase reporter assays, co-immunoprecipitation, and ubiquitination assays to resolve the TGF-β1/Smad3–USP7–Snail1 pathway.
Tested the therapeutic efficacy of pharmacological interventions, including the small-molecule USP7-interacting compound Olaparib, in cell culture and in vivo adhesion models.
Smad3 activation downstream of TGF-β1 transcriptionally upregulated USP7, which directly deubiquitinated and stabilized Snail1 protein to promote macrophage-to-myofibroblast transition.
Knockdown of Usp7 or inhibition of Smad3 prevented macrophage transition into myofibroblast-like cells and markedly reduced postoperative peritoneal adhesion formation in mice.
Olaparib disrupted the binding of USP7 to Snail1, enhanced ubiquitin-dependent Snail1 degradation, and attenuated adhesion severity in vivo in a dose-responsive manner.

Cite This Study

Gan et al. (2026) studied this question.

synapsesocial.com/papers/6aa7b2e10926e14a848b1667 https://doi.org/10.1186/s10020-026-01638-7

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September 14, 2026Molecular MedicineOpen Access

USP7-mediated stabilization of Snail1 drives macrophage-to-myofibroblast transition and promotes postoperative peritoneal adhesions

View Full Paper

Ask AI

Bookmark

Authors

LGLi Gan SZSihan Zhao BHBowen Huo

Discussion

Member takes

Overview

Preclinical study demonstrates that USP7 stabilizes Snail1 to drive macrophage transition into myofibroblasts, indicating that targeting USP7 alleviates postoperative adhesions.

Key Points

To determine the cellular origins of myofibroblast accumulation in postoperative peritoneal adhesions and characterize the molecular signaling pathway driving macrophage-to-myofibroblast transition.
Established a mouse model of postoperative peritoneal adhesions and used immortalized bone marrow-derived macrophages to model macrophage-to-myofibroblast transition in vitro.
Performed transcriptome sequencing, RNA interference, dual-luciferase reporter assays, co-immunoprecipitation, and ubiquitination assays to resolve the TGF-β1/Smad3–USP7–Snail1 pathway.
Tested the therapeutic efficacy of pharmacological interventions, including the small-molecule USP7-interacting compound Olaparib, in cell culture and in vivo adhesion models.
Smad3 activation downstream of TGF-β1 transcriptionally upregulated USP7, which directly deubiquitinated and stabilized Snail1 protein to promote macrophage-to-myofibroblast transition.
Knockdown of Usp7 or inhibition of Smad3 prevented macrophage transition into myofibroblast-like cells and markedly reduced postoperative peritoneal adhesion formation in mice.
Olaparib disrupted the binding of USP7 to Snail1, enhanced ubiquitin-dependent Snail1 degradation, and attenuated adhesion severity in vivo in a dose-responsive manner.

Cite This Study

Gan et al. (2026) studied this question.

synapsesocial.com/papers/6aa7b2e10926e14a848b1667 https://doi.org/10.1186/s10020-026-01638-7

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