Abstract
Protein kinase C (PKC) is a protein kinase with important cellular functions. PKC-δ, a member of the novel PKC subfamily, has been well-documented over the years. Activation of PKC-δ plays an important regulatory role in myocardial ischemia/reperfusion (IRI) injury and myocardial fibrosis, and its activity and expression levels can regulate pathological cardiovascular diseases such as atherosclerosis, hypertension, cardiac hypertrophy, and heart failure. This article aims to review the structure and function of PKC-δ, summarize the current research regarding its activation mechanism and its role in cardiovascular disease, and provide novel insight into further research on the role of PKC-δ in cardiovascular diseases.
Highlights
The term cardiovascular disease (CVD) includes many different diseases, such as coronary heart disease, hypertension, heart failure, and atherosclerosis [1]
These results suggest that inhibition of protein kinase C (PKC)-δ translocation inhibits apoptosis induced by reperfusion injury
Ang II increases Connective tissue growth factor (CTGF) expression in vivo [122]. He et al directly tested the regulation of CTGF expression by PKC-δ isoform activation after Ang II stimulation in vitro and in vivo, and the results indicated that PKC-δ inhibition may aggravate the expression of CTGF and potential fibrosis [123]
Summary
The term cardiovascular disease (CVD) includes many different diseases, such as coronary heart disease, hypertension, heart failure, and atherosclerosis [1]. The treatment of cardiovascular diseases has greatly improved in recent years, these diseases still exhibit high morbidity and mortality. Studies have found that protein kinase C (PKC) plays a multifaceted role in the pathophysiology of heart development and many cardiovascular diseases. 10 PKC family members have been found in mammalian tissues. These family members can be divided into three categories according to their dependency on lipid second messengers and calcium and ion coactivators for activation: conventional PKCs (α, β1, β2, γ), novel PKCs (δ, ε, η, θ), and atypical PKCs (ζ, λ/ι) [3–5]. The activation of conventional PKCs requires diglyceride (DAG), phosphatidylserine (PS), and Ca2+.
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