Abnormal phosphorylation / dephosphorylation and Ca 2+ dysfunction in heart failure

Heart failure (HF) can be caused by a variety of causes characterized by abnormal myocardial systole and diastole. Ca current through the L-type calcium channel (LTCC) on the membrane is the initial trigger signal for a cardiac cycle. Declined systole and diastole in HF are associated with dysfuncti...

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Bibliographic Details
Published inHeart failure reviews Vol. 29; no. 4; p. 751
Main Authors Liu, Yan-Bing, Wang, Qian, Song, Yu-Ling, Song, Xiao-Min, Fan, Yu-Chen, Kong, Lin, Zhang, Jing-Sai, Li, Sheng, Lv, Yi-Ju, Li, Ze-Yang, Dai, Jing-Yu, Qiu, Zhen-Kang
Format Journal Article
LanguageEnglish
Published United States 01.07.2024
Subjects
Calcium - metabolism
Calcium Channels, L-Type - metabolism
Endoplasmic Reticulum - metabolism
Heart Failure - metabolism
Heart Failure - physiopathology
Humans
Myocardium - metabolism
Myofibrils - metabolism
Phosphorylation
Heart failure
Phosphorylation
Ca2
L-type calcium channel
Endoplasmic reticulum
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Summary:Heart failure (HF) can be caused by a variety of causes characterized by abnormal myocardial systole and diastole. Ca current through the L-type calcium channel (LTCC) on the membrane is the initial trigger signal for a cardiac cycle. Declined systole and diastole in HF are associated with dysfunction of myocardial Ca function. This disorder can be correlated with unbalanced levels of phosphorylation / dephosphorylation of LTCC, endoplasmic reticulum (ER), and myofilament. Kinase and phosphatase activity changes along with HF progress, resulting in phased changes in the degree of phosphorylation / dephosphorylation. It is important to realize the phosphorylation / dephosphorylation differences between a normal and a failing heart. This review focuses on phosphorylation / dephosphorylation changes in the progression of HF and summarizes the effects of phosphorylation / dephosphorylation of LTCC, ER function, and myofilament function in normal conditions and HF based on previous experiments and clinical research. Also, we summarize current therapeutic methods based on abnormal phosphorylation / dephosphorylation and clarify potential therapeutic directions.
ISSN:1573-7322