Abstract
HIV-1-associated nephropathy (HIVAN) is a rapidly progressive form of focal segmental glomerulosclerosis. HIV transgenic mice can develop a HIVAN-like renal disease. Zhong et al. show that the oral administration of a cyclic nucleotide phosphodiesterase 4 inhibitor and a retinoic acid receptor-α agonist can prevent the development of HIVAN in transgenic mice, acting through a cAMP-dependent mechanism that is independent of HIV-1 genes. These findings suggest that endogenous host factors play a critical role in HIVAN.
Publication types
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Research Support, N.I.H., Extramural
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Comment
MeSH terms
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AIDS-Associated Nephropathy / prevention & control*
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Aminopyridines / pharmacology*
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Animals
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Benzamides / pharmacology*
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Benzoates / pharmacology*
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Cyclopropanes / pharmacology
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Female
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HIV Infections / drug therapy*
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HIV-1 / genetics*
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Kidney Tubules / drug effects*
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Male
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Phosphodiesterase 4 Inhibitors / pharmacology*
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Renal Insufficiency / prevention & control*
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Tetrahydronaphthalenes / pharmacology*
Substances
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Aminopyridines
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Benzamides
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Benzoates
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Cyclopropanes
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Phosphodiesterase 4 Inhibitors
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Tetrahydronaphthalenes
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Roflumilast
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Am 580