TPM2 regulates contractility and biomechanical properties in trabecular meshwork cells.

ABSTRACT: The contraction-relaxation balance of trabecular meshwork (TM) cells is a critical physiological mechanism regulating aqueous humor outflow resistance. Both hypercontractility and impaired relaxation of TM cells can obstruct aqueous humor outflow. Such pathological changes not only directly compromise outflow function but may also reduce the clinical efficacy of ocular hypotensive therapies. However, the molecular regulatory mechanisms underlying TM cell contractility remain incompletely understood. Based on single-cell RNA sequencing data previously generated by our group, our analyses revealed abnormal expression patterns of tropomyosin family members (TPMs) in major TM cell subpopulations in primates with primary open-angle glaucoma (POAG). This study investigated the effects of TPM2 in

SUBMITTER: Shen B 

PROVIDER: S-EPMC12635119 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature