Enhancing trabecular outflow by disrupting the actin cytoskeleton, increasing uveoscleral outflow with prostaglandins, and understanding the pathophysiology of presbyopia. Interrogating Mother Nature: asking why, asking how, recognizing the signs, following the trail

Experimental Eye Research

Volumn 86, Issue 1, 2008, Pages 3-17

  Kaufman, Paul L ^a  

^a UNIVERSITY OF WISCONSIN SCHOOL OF MEDICINE AND PUBLIC HEALTH   (United States)

Author keywords

ciliary muscle; cytoskeleton; gene therapy; intraocular pressure; outflow facility; presbyopia; trabecular meshwork; uveoscleral outflow

Indexed keywords

ACETYLCHOLINE; ACTIN; MATRIX METALLOPROTEINASE; MUSCARINIC RECEPTOR; PROSTAGLANDIN F2 ALPHA DERIVATIVE;

ACCOMMODATION; CELL ADHESION; CILIARY MUSCLE; CYTOSKELETON; GENE THERAPY; HUMAN; INTRAOCULAR PRESSURE; NONHUMAN; PATHOPHYSIOLOGY; PRESBYOPIA; PRIORITY JOURNAL; REVIEW; SCLERA; SYMPTOMATOLOGY; UVEA;

ACCOMMODATION, OCULAR; ACTINS; ANIMALS; AQUEOUS HUMOR; CILIARY BODY; CYTOSKELETON; GENE THERAPY; HUMANS; INTRAOCULAR PRESSURE; PRESBYOPIA; PROSTAGLANDINS; SCLERA; TRABECULAR MESHWORK;

EID: 36849053984     PISSN: 00144835     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.exer.2007.10.007     Document Type: Review

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