摘要
Statins inhibit the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, and hence have a profound effect in lowering serum cholesterol. Their predominant clinical use to date is in primary and secondary prevention of cardiovascular disease. However recently interest has developed regarding the so-called “pleiotropic” effects of statins—these drugs have significant anti-fibrotic, anti-inflammatory, and immunomodulatory properties. Such effects of statins have already been shown to be beneficial in modulating the pathological mechanisms involved in pul-monary fibrosis, renal disease, non-ischaemic cardiac failure, and tissue scarring. Many of these actions are mediated by inhibition of the Rho kinase pathway. Epidemiological studies suggest that patients who take statins have a lower risk of developing glaucoma, and lower rates of glaucoma progression. Here, we review what is known about the pleiotropic effect of statins to date, and examine how these effects may modulate the molecular mechanisms involved in glaucoma pathogenesis.
Statins inhibit the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, and hence have a profound effect in lowering serum cholesterol. Their predominant clinical use to date is in primary and secondary prevention of cardiovascular disease. However recently interest has developed regarding the so-called “pleiotropic” effects of statins—these drugs have significant anti-fibrotic, anti-inflammatory, and immunomodulatory properties. Such effects of statins have already been shown to be beneficial in modulating the pathological mechanisms involved in pul-monary fibrosis, renal disease, non-ischaemic cardiac failure, and tissue scarring. Many of these actions are mediated by inhibition of the Rho kinase pathway. Epidemiological studies suggest that patients who take statins have a lower risk of developing glaucoma, and lower rates of glaucoma progression. Here, we review what is known about the pleiotropic effect of statins to date, and examine how these effects may modulate the molecular mechanisms involved in glaucoma pathogenesis.
