Fig. 2

RNA related mechanism of cardiac hypertrophy. Recent studies on RNA creates a novel regulatory network for cardiac hypertrophy. (I) Long non-coding RNAs (lncRNAs) are molecularly multi-functional. They can physically interact with and modulate function of cytoplasmic protein, chromatin remodeling factors, and transcription factors. (II) MicroRNAs (miRNAs) target mRNA and suppressed its expression. Circular RNAs (circRNAs) are also multifunctional, but cardiac hypertrophy related researches mainly focuses on their role as miRNA sponges. (III) RNA modification further adds to the complexity of the regulatory network. N6-methyladenosine (m6A) alters the function of mRNA. Modulating m6A “writer” or “eraser” can affect the development of cardiac remodeling. Oxidative stress creates 8-oxoguanine modification on miR-1, which leads to its target mismatch and triggers hypertrophic response. miRNA: microRNA; circRNA: circular RNA; ZFAS1: Zinc finger antisense 1; PRC2: polycomb repressor complex 2; Chaer: cardiac-hypertrophy-associated epigenetic regulator; SERCA2a: sarco/endoplasmic reticulum Ca2+-ATPase 2a; CPhar: cardiac physiological hypertrophy-associated regulator; TF: transcription factor; RISC: RNA Induced Silencing Complex; HRCR: heart-related circRNA; ROS: reactive oxygen species; WTAP: Wilms’ tumor 1-associating protein; METTL3: methyltransferase like 3; METTL14: methyltransferase like 14; m6A: N6-methyladenosine; FTO: fat mass and obesity associated gene; PE: Phenylephrine; ISO: isoprenaline