Abstract
Heart failure is a major cause of death and disability. Impairments
in blood circulation that accompany heart failure can be traced,
in part, to alterations in the activity of the sarcoplasmic reticulum
Ca$^2+$ pump that are induced by its interactions with phospholamban,
a reversible inhibitor. If phospholamban becomes superinhibitory
or chronically inhibitory, contractility is diminished, inducing
dilated cardiomyopathy in mice and humans. In mice, phospholamban
seems to encumber an otherwise healthy heart, but humans with a phospholamban-null
genotype develop early-onset dilated cardiomyopathy.
- 12838339
- animals,
- atpase,
- calcium-binding
- cardiomyopathy,
- contraction,
- dilated,
- gov't,
- humans,
- knockout,
- mice,
- myocardial
- non-u.s.
- p.h.s.,
- proteins,
- research
- reticulum,
- sarcoplasmic
- support,
- u.s.
- {c}a$^{2+}$-transporting
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