**2. Kruppel-Like Factor 15 and Cardiac Hypertrophy**

KLF15 is one member of a family of 18 Kruppel-like factors (KLF). The KLFs are a subclass of the zinc-finger family of DNA-binding transcriptional regulators, homologous to the *Drosophila* gap gene Kruppel [11]. KLF15 is expressed in myocytes and fibroblasts [12]. Both in vitro and in vivo studies support a role for KLF15 as a repressor of pathological cardiac hypertrophy and fibrosis [10,12,13]. Cardiac KLF15 expression is low during development and increases after birth to reach high levels in the adult rat and mouse heart [13,14]. The action of KLF15 to repress hypertrophy occurs through the inhibition of the activity of pro-hypertrophic transcriptional regulators, which affect atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) promoter activity [13]. Expression of KLF15 is unchanged during physiologically induced LVH (i.e., exercise) but is decreased in pathological LVH [15].

Table 1 summarizes the results from in vivo studies that have explored KLF15 in experimental models of cardiac hypertrophy. Overall, regardless of the model used, the results have consistently shown that loss of KLF15 contributes to the development of cardiac hypertrophy. The approaches used to induce LVH include cardiac KLF15 null (−/−) mice, high blood pressure (angiotensin (Ang) II infusion [10], transgenic TGR(mRen2)27 rat (Ren-2) [15], high salt diet in Dahl salt-sensitive rats, isoproterenol infusion [16]) and surgical methods such as transaortic constriction [13], ascending aortic constriction [12,13], and aortic banding [17].
