[HTML][HTML] Left ventricular hypertrophy in renal disease: beyond preload and afterload
E Ritz - Kidney international, 2009 - Elsevier
E Ritz
Kidney international, 2009•ElsevierTo 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.
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.
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.
Elsevier