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The interfacial synergy effect caused by the space charge transfer of heterojunctions can effectively modify the catalytic activity. Herein, a composite heterojunction catalyst of CoTe 2 /CoP with moderate Gibbs free energy of hydrogen adsorption is designed based on interfacial effects driven by work function difference between CoTe 2 and CoP. As expected, CoTe 2 /CoP only needs overpotentials of 80 mV at 10 mA cm−2 and stability for continuous catalysis at the current density of 100 mA cm−2 for 20 h in hydrogen evolution reaction (HER). The experimental results and theory calculations identify that the built-in field drives the transfer of electrons from CoTe 2 to CoP at the interface, which realizes electronic redistribution with increased electron density on the Co atoms in CoP and optimizes the adsorption-free energy of the reaction intermediates, thereby, accelerating HER kinetics. Besides, the CoTe 2 /CoP heterostructure also behaves the excellent catalytic activity towards water splitting. [Display omitted] • CoTe 2 /CoP is prepared via one-step phosphotellurization method. • Built-in field drives the transfer of electrons from CoTe 2 to CoP at the interface. • Electronic redistribution optimizes the adsorption-free energy of the reaction intermediates. • CoTe 2 /CoP exhibits the boosted hydrogen evolution reaction (HER) performance. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases are the leading cause of death worldwide. During the development of cardiovascular diseases, hypoxia plays a crucial role. Hypoxia-inducible factors (HIFs) are the key transcription factors for adaptive hypoxic responses, which orchestrate the transcription of numerous genes involved in angiogenesis, erythropoiesis, glycolytic metabolism, inflammation, and so on. Recent studies have dissected the precise role of cell-specific HIFs in the pathogenesis of hypertension, atherosclerosis, aortic aneurysms, pulmonary arterial hypertension, and heart failure using tissue-specific HIF-knockout or -overexpressing animal models. More importantly, several compounds developed as HIF inhibitors or activators have been in clinical trials for the treatment of renal cancer or anemia; however, little is known on the therapeutic potential of these inhibitors for cardiovascular diseases. The purpose of this review is to summarize the recent advances on HIFs in the pathogenesis and pathophysiology of cardiovascular diseases and to provide evidence of potential clinical therapeutic targets. [ABSTRACT FROM AUTHOR]