User:Alicia Daeden/Sandbox 130: Difference between revisions
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Common treatment schemes of heart failure modify levels of cytosolic Ca2+. This provides immediate improvement in heart function, but it can lead to serious side effects if used for an extended period of time. Drugs that alter the Ca2+ sensitivity of the thin filament rather than the cytosolic Ca2+ concentration, provide a safer alternative. | Common treatment schemes of heart failure modify levels of cytosolic Ca2+. This provides immediate improvement in heart function, but it can lead to serious side effects if used for an extended period of time. Drugs that alter the Ca2+ sensitivity of the thin filament rather than the cytosolic Ca2+ concentration, provide a safer alternative. | ||
An increase in Ca2+ sensitivity would be beneficial for the treatment of heart failure, whereas the use of Ca2+ desentizers may provide protection against the development of hypertrophic cardiomyopathy (HCM). | An increase in Ca2+ sensitivity would be beneficial for the treatment of heart failure, whereas the use of Ca2+ desentizers may provide protection against the development of hypertrophic cardiomyopathy (HCM). | ||
EGCg has a role as Ca2+ desensitizer and is particularly interesting in regards to treatment for HCM because that is a scavenger of radicals and this may help treat or prevent HCM by sequestering reactive oxygen species as well as by inhibiting ATPases activity (this prevents binding of Ca2+ so there is no ATPase activity). | EGCg has a role as Ca2+ desensitizer and is particularly interesting in regards to treatment for HCM because that is a scavenger of radicals and this may help treat or prevent HCM by sequestering reactive oxygen species as well as by inhibiting ATPases activity (this prevents binding of Ca2+ so there is no ATPase activity). | ||