Our cryo-EM structural data, together with the single-molecule magnetic tweezers analysis, reveal that the plant actin filament from Zea mays pollen is more str

Heart failure is a major health issue that threatens life and health. Previous studies have shown that heart failure is the terminal stage of arrhythmia, dilated cardiomyopathy, hypertension, hypertrophic cardiomyopathy and myocardial infarction. The pathological mechanisms through which cardiovascular diseases result in heart failure include myocardial fibrosis and hypertrophy, myocardial cell death, mitochondrial dysfunction, vascular remodeling and calcium dysregulation. However, the detailed molecular mechanisms of heart failure remain elusive because of its complexity, hindering the development of intervention approaches for heart failure. The present study reviewed recent research progress on heart failure and provided references and strategies for the prevention and treatment of heart failure.

Cilia are microtubule‐based organelles found on the surfaces of many types of cells, including cardiac fibroblasts, vascular endothelial cells, human retinal pigmented epithelial‐1 (RPE‐1) cells, and alveolar epithelial cells. These organelles can be classified as immotile cilia, referred to as primary cilia in mammalian cells, and motile cilia. Primary cilia are cellular sensors that detect extracellular signals; this is a critical function associated with ciliopathies, which are characterized by the typical clinical features of developmental disorders. Cilia are extensively studied organelles of the microtubule cytoskeleton. However, the ciliary actin cytoskeleton has rarely been studied. Clear evidence has shown that highly regulated actin cytoskeleton dynamics contribute to normal ciliary function. Actin‐binding proteins (ABPs) play vital roles in filamentous actin (F‐actin) morphology. Here, we discuss recent progress in understanding the roles of ABPs in ciliary structural remodeling and further downstream ciliary signaling with a focus on the molecular mechanisms underlying actin cytoskeleton‐related ciliopathies.