Although the mechanism by which Morrbid participates in cardiac hypertrophy remains unclear, studies have reported that Morrbid is significantly downregulated in transverse aortic constriction (TAC) mice with adenosine receptor A2A overexpression, suggesting that Morrbid may mediate the cardioprotective effect of A2A or directly participate in the pathological process of cardiac hypertrophy [106]. Here, MIR4435-2HG is linked to cardiac hypertrophy.