Author(s): Ritz E
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Abstract To explain ventricular concentric and/or eccentric hypertrophy in chronic kidney disease, past studies suggested that this was the result of increased preload and/or afterload. Using a renal ablation model of the mouse with documented absence of hypertension, Siedlecki et al. provide evidence for the involvement of the mammalian target of rapamycin (mTOR) pathway. This suggests that load-independent primary stimuli trigger or contribute to ventricular hypertrophy and fibrosis in uremia.
This article was published in Kidney Int
and referenced in Journal of Clinical & Experimental Cardiology