Research progress on the molecular mechanisms of heart failure with preserved ejection fraction

Heart failure with preserved ejection fraction (HFpEF) is a clinical syndrome with multiple phenotypes and high heterogeneity, which is a serious threat to human health. Its pathophysiology and cellular molecular mechanisms involve multiple systems and have not yet been elucidated,thus impeding the discovery and development of mechanism-based therapies. At present, it is more common to believe that systemic inflammatory states caused by cardiovascular diseases and other systemic comorbidities drive cardiac structural remodeling and diastolic and systolic function changes through multiple signaling pathways, which is the basic paradigm of HFpEF. HFpEF have complex cellularand molecular mechanisms involving multiple aspects and links of cellular activity. This review focuses on the progress of molecular pathological mechanisms of HFpEF from three aspects: NO-cGMP-PKG pathway, oxidative-nitrosative stress and mitochondrial metabolism. It is of great value and significance for the development of therapeutic drugs for this disease.