Key result
Endogenous adrenomedullin deficiency in AM+/- mice led to significantly more pronounced cardiac hypertrophy, fibrosis, and renal damage following cardiovascular stress compared to wild-type mice.
Why the study?
Does endogenous adrenomedullin protect against stress-induced cardiac hypertrophy, fibrosis, and renal damage in mice?
Population
Mice heterozygous for an AM-null mutation and their wild-type littermates; cardiac myocytes from neonates
Comparison
Aortic constriction or angiotensin II infusion… vs Wild-type littermates subjected to the same…
Design
Preclinical
Authors
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Does not support clinical adrenomedullin modulation; leaves open its therapeutic targeting in human cardiac and renal stress.
Does endogenous adrenomedullin protect against stress-induced cardiac hypertrophy, fibrosis, and renal damage in mice?
Endogenous adrenomedullin exerts a protective effect against stress-induced cardiac hypertrophy and renal damage via PKC- and PKA-dependent regulation of ERK activation in a mouse model.
Niu et al. (2004) studied Cardiac hypertrophy, fibrosis, and renal damage. AM-null mutation (AM+/-) vs. Wild-type littermates was evaluated on Cardiac hypertrophy, fibrosis, and renal damage. Endogenous adrenomedullin deficiency in AM+/- mice led to significantly more pronounced cardiac hypertrophy, fibrosis, and renal damage following cardiovascular stress compared to wild-type mice.
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