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https://www.selleckchem.com/ Despite recent advances in chronic heart failure management (either pharmacological or non-pharmacological), the prognosis of heart failure (HF) patients remains poor. This poor prognosis emphasizes the need for developing novel pathways for testing new HF drugs, beyond neurohumoral and hemodynamic modulation approaches. The development of new drugs for HF therapy must thus necessarily focus on novel approaches such as the direct effect on cardiomyocytes, coronary microcirculation, and myocardial interstitium. This review summarizes principal evidence on new possible pharmacological targets for the treatment of HF patients, mainly focusing on microcirculation, cardiomyocyte, and anti-inflammatory therapy.Despite treatments being improved and many risk factors being identified, cardiovascular disease (CVD) is still a leading cause of mortality and disability worldwide. N6-methyladenosine (m6A) is the most common, abundant, and conserved internal modification in RNAs and plays an important role in the development of CVD. Many studies have shown that aabnormal m6A modifications of coding RNAs are involved in the development of CVD. In addition, non-coding RNAs (ncRNAs) exert post-transcriptional regulation in many diseases including CVD. Although ncRNAs have also been found to be modified by m6A, the studies on m6A modifications of ncRNAs in CVD are currently lacking. In this review, we summarized the recent progress in understanding m6A modifications in the context of coding RNAs and ncRNAs, as well as their regulatory roles in CVD.Rationale Decreased expression and activity of endothelial nitric oxide synthase (eNOS) in response to inflammatory and metabolic insults is the hallmark of endothelial cell (EC) dysfunction that preludes the development of atherosclerosis and hypertension. We previously reported the atheroprotective properties of the ubiquitin-editing and anti-inflammatory protein A20, also known as TNFAIP3, in part through int

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