**1. Introduction**

Left ventricular hypertrophy (LVH) is an independent and potent risk factor for cardiovascular events [1] and is often present in patients with hypertension. LVH is diagnosed by electrocardiography, echocardiography or cardiac magnetic resonance imaging. The prevalence of LVH in the general population is 10% [1] but rises to 40–70% in those with risk factors such as hypertension, aortic stenosis, diabetes and chronic kidney disease [2–5]. As LVH per se causes no symptoms (preclinical), it is often only diagnosed after patients present with symptoms such as heart failure [1]. Treatment to regress LVH is key to improving health outcomes [6,7], but currently available drugs have only modest cardioprotective effects [8]. Improved understanding of the molecular mechanisms that contribute to the development of LVH provides an opportunity to identify pathways that may be new therapeutic targets.

Our group is interested in the function and regulation of transcription factors in the development of LVH. To date, studies have mainly focused on factors that induce hypertrophy such as GATA binding protein 4 (GATA4), myocyte enhancer factor 2 (MEF2) and serum response factor (SRF) [9] (Figure 1). However, there are also transcriptional repressors of hypertrophy such as Kruppel-like factor 15 (KLF15) [10], and compelling experimental evidence that suppression of KLF15 contributes to LVH through lack of inhibition of pro-hypertrophic transcription factors [9]. This review provides a summary of 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.

**Figure 1.** Schema illustrating how loss of the inhibitory effect of KLF15 on pro-hypertrophic cardiac transcriptional regulators may contribute to the development of LVH and heart failure. *↑* Increased; X in red font represents the inhibitory effect; GATA4, GATA binding protein 4; KLF15, Kruppel-like factor 15; MEF2, myocyte enhancer factor 2; SRF, serum response factor.
