Key result
Nitric oxide and natriuretic peptides act as endogenous inhibitors of maladaptive cardiac hypertrophy signalling, helping to control the balance between adaptation and heart failure.
Highlights the potential of targeting maladaptive hypertrophy signalling pathways, such as those involving nitric oxide, for future therapeutic strategies in cardiac disease.
In pathological conditions associated with persistent increases in hemodynamic workload (old myocardial infarction, high blood pressure, valvular heart disease), a number of signalling pathways are activated in the heart, all of which promote hypertrophic growth of the heart, characterised at the cellular level by increases in individual cardiac myocyte size. Some of these pathways are required for a successful adaptation to cardiac injury. Other pathways are maladaptive, however, as they lead to progressive contractile dysfunction and heart failure. The free radical gas nitric oxide and natriuretic peptides, both of which are produced in the heart, have emerged as endogenous inhibitors of maladaptive hypertrophy signalling. Overall, it appears that cardiac hypertrophy is controlled by an interplay of pro- and antihypertrophic signalling networks. This delicate balance can tip towards adaptation or heart failure. In the future, patients living with cardiac disease may benefit from therapeutic strategies targeting maladaptive hypertrophy signalling pathways.
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Kempf et al. (2004) conducted a review in Cardiac hypertrophy. Nitric oxide and natriuretic peptides was evaluated. Nitric oxide and natriuretic peptides act as endogenous inhibitors of maladaptive cardiac hypertrophy signalling, helping to control the balance between adaptation and heart failure.
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