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Background Left ventricular hypertrophy(LVH) induced by systemic hypertension represents a maladaptive response to the increased overload. However antihypertensive treatments are not always useful to regress or prevent LVH. Thoroughly understanding the mechanisms will help to find new therapeutic targets that prevent or reverse left ventricular hypertrophy. A number of regulators and molecular signaling pathways have been shown to be involved in the hypertrophic process, such as angiotensin II, heat shock proteins 90, micro RNAs, TRPC,m TOR, HDAC and PI3K/Akt signaling pathways. Therefore, other treatments, such as G1 cyclin antagonists,HSP90 inhibitor,Rho-kinase inhibitor, calcineurin blockers, CS866, statins, scutellarin, and aldosterone antagonist could prevent left ventricular hypertrophy.
Background Left ventricular hypertrophy (LVH) induced by systemic hypertension represents a maladaptive response to the increased overload. However antihypertensive treatments are not always useful to regress or prevent LVH. Thoroughly understanding the mechanisms will help to find new therapeutic targets that prevent or reverse left ventricular A number of regulators and molecular signaling pathways have been shown to be involved in the hypertrophic process, such as angiotensin II, heat shock proteins 90, micro RNAs, TRPC, m TOR, HDAC and PI3K / Akt signaling pathways. Thus, other treatments, such as G1 cyclin antagonists, HSP90 inhibitor, Rho-kinase inhibitor, calcineurin blockers, CS866, statins, scutellarin, and aldosterone antagonist could prevent left ventricular hypertrophy.