Abstract: Primary angle-closure glaucoma (PACG) is a vision-threatening eye disease that can lead to blindness, and its pathogenesis has long been debated. Traditionally, anatomical factors such as iris bombe, anterior lens displacement, and anterior rotation of the ciliary body have been considered the primary causes. However, the inconsistent therapeutic outcomes targeting these structural abnormalities suggest that they may represent concomitant changes during disease progression rather than the fundamental cause. Drawing from this insight, this article explores how intraocular chamber pressure imbalances, triggered by abnormal intraocular fluid circulation, affect different intraocular structures and functions, with the goal of clarifying the pathophysiological mechanisms underlying the development and progression of PACG. The proposed mechanisms mainly include: pathological choroidal expansion or abnormal suprachoroidal fluid transport leading to altered choroidal-vitreous pressure; abnormalities of the ciliary body-zonules-crystalline lens-hyaloid-anterior vitreous complex (CZLHV) resulting in changes in vitreous cavity-posterior chamber pressure; and forward displacement of the CZLHV complex compressing the iris, thereby creating a posterior-anterior chamber pressure gradient. This sequence ultimately causes iridotrabecular contact, angle closure, and obstruction of aqueous humor outflow through the trabecular meshwork. By systematically summarizing the roles of choroidal expansion, the vitreous buffering system, and the CZLHV complex in the pathogenesis and progression of PACG, this article aims to provide new insights for precision management and future pathogenesis research in PACG.

Key words: Primary angle-closure glaucoma, Intraocular fluid circulation, Choroidal expansion, Vitreous buffering system, Ciliary body-zonules-crystalline lens-hyaloid-anterior vitreous complex