Currently, chronic heart failure (CHF) is stratified into HF with reduced ejection fraction (HFrEF) and HF with preserved EF (HFpEF). During last two decades, a number of evidence were accumulated that the over activation of intracellular signaling pathways downstream of the sympathetic nerve activity (SNA) and the renin-angiotensin-aldosterone (RAA) system, which leads to abnormalities of Ca⁺⁺ handling, myocyte hypertrophy, myocyte cell death, and/or interstitial fibrosis, contributes to the development of HFrEF. Nevertheless, the prognosis of HFrEF is still poor even in patients who are treated with sufficient dose of RAS inhibitors and β adrenergic receptor blockers, the first line drugs for HFrEF. In the case of HFpEF, recent studies elucidated the prognosis is as poor as HFrEF and no effective drugs have been proven to improve the prognosis to date, probably which results from the lack of understanding of the molecular mechanisms for HFpEF. In this context, the symposium welcomes new findings and thoughts of molecular mechanisms of development or progression of either HFrEF or HFpEF.