Abstract
Left ventricular hypertrophy (LVH) is an independent risk factor for adverse cardiovascular events and is often present in patients with hypertension. Treatment to reduce blood pressure and regress LVH is key to improving health outcomes, but currently available drugs have only modest cardioprotective effects. Improved understanding of the molecular mechanisms involved in the development of LVH may lead to new therapeutic targets in the future. There is now compelling evidence that the transcription factor Kruppel-like factor 15 (KLF15) is an important negative regulator of cardiac hypertrophy in both experimental models and in man. Studies have reported that loss or suppression of KLF15 contributes to LVH, through lack of inhibition of pro-hypertrophic transcription factors and stimulation of trophic and fibrotic signaling pathways. This review provides a summary of the experimental and human studies that have investigated the role of KLF15 in the development of cardiac hypertrophy. It also discusses our recent paper that described the contribution of genetic variants in KLF15 to the development of LVH and heart failure in high-risk patients.
Highlights
Left ventricular hypertrophy (LVH) is an independent and potent risk factor for cardiovascular events [1] and is often present in patients with hypertension
Aortic banding increased ejection fraction and LV pressure compared to the sham group, and both improved after debanding. At both 3 and 6-weeks after aortic banding, rats had decreased Kruppel-like factor 15 (KLF15) mRNA, and increased connective tissue growth factor (CTGF), transforming growth factor-β (TGFβ) and myocardin-related transcription factor A (MRTF-A) with fibrosis and increased collagen I and III mRNA compared to sham-operated rats
We recently explored the genetic association of KLF15 single nucleotide polymorphisms (SNP) in patients with type 2 diabetes and an echocardiographic assessment of LV
Summary
Left ventricular hypertrophy (LVH) is an independent and potent risk factor for cardiovascular events [1] and is often present in patients with hypertension. As LVH per se causes no symptoms (preclinical), it is often only diagnosed after patients present with symptoms such as heart failure [1]. This review provides a summary of experimental and human studies that have investigated the role of KLF15 in the. 2018, 19, 1303 review provides a summary of experimental and human studies that have investigated the role of KLF15 in the development of cardiac hypertrophy. It discusses our recent paper that described the contribution of genetic variants inItKLF15 to the development of LVH heart the failure in highdevelopment of cardiac hypertrophy. Of genetic variants in KLF15 to the development of LVH and heart failure in high-risk patients
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