Mitochondrial-Targeted Antioxidants Attenuate TGF-β2 Signaling in Human Trabecular Meshwork Cells | Zendy

Vidhya R. Rao | Zendy; Jonathan D. Lautz | Zendy; Simon Kaja | Zendy; Eileen M. Foecking | Zendy; Emoke Lukács | Zendy; Evan B. Stubbs | Zendy

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Mitochondrial-Targeted Antioxidants Attenuate TGF-β2 Signaling in Human Trabecular Meshwork Cells

Author(s) -

Vidhya R. Rao,

Jonathan D. Lautz,

Simon Kaja,

Eileen M. Foecking,

Emoke Lukács,

Evan B. Stubbs

Publication year - 2019

Publication title -

investigative ophthalmology and visual science

Language(s) - Uncategorized

Resource type - Journals

SCImago Journal Rank - 1.935

H-Index - 218

eISSN - 1552-5783

pISSN - 0146-0404

DOI - 10.1167/iovs.19-27542

Subject(s) - trabecular meshwork , ctgf , oxidative stress , extracellular matrix , reactive oxygen species , transforming growth factor , smad , extracellular , chemistry , microbiology and biotechnology , immunocytochemistry , mitochondrion , growth factor , biology , endocrinology , biochemistry , glaucoma , receptor , neuroscience

POAG is a progressive optic neuropathy that is currently the leading cause of irreversible blindness worldwide. While the underlying cause of POAG remains unclear, TGF-β2-dependent remodeling of the extracellular matrix (ECM) within the trabecular meshwork (TM) microenvironment is considered an early pathologic consequence associated with impaired aqueous humor (AH) outflow and elevated IOP. Early studies have also demonstrated markedly elevated levels of oxidative stress markers in AH from POAG patients along with altered expression of antioxidant defenses. Here, using cultured primary or transformed human TM cells, we investigated the role oxidative stress plays at regulating TGF-β2-mediated remodeling of the ECM.

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