Glomerular sclerotic lesions develop when the glomerular filtration surface area exceeds the
availability of podocyte foot process coverage, but the mechanisms involved are
incompletely characterized. We evaluated potential mechanisms using a transgenic
(podocin promoter-AA-4E-BP1) rat in which podocyte capacity for hypertrophy in response
to growth factor/nutrient signaling is impaired. FSGS lesions resembling human FSGS
developed spontaneously by 7 months of age, and could be induced earlier by accelerating …