Contractile proteins of the heart.
Research findings to date indicate that there may not be a discrete change in contractile proteins in the common forms of heart failure. While the search for a defective myosin molecule in this context no longer seems promising, it remains plausible to propose "up-regulation" to a myosin variant with high ATPase activity as a means of increasing contractility in the failing heart.
D000251:Adenosine Triphosphatases / Q000502:physiology; D000818:Animals; D006321:Heart / Q000502:physiology*; D006333:Heart Failure / Q000503:physiopathology; D006801:Humans; D007527:Isoenzymes / Q000502:physiology*; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000201:enzymology; D009218:Myosins / Q000502:physiology*; D011817:Rabbits; D051381:Rats; D013963:Thyroid Hormones / Q000502:physiology
D007527:Isoenzymes; D013963:Thyroid Hormones; D000251:Adenosine Triphosphatases; D009218:Myosins