Abstract
Insufficient oxygen availability (hypoxia) is a precursor to numerous cardiovascular diseases, including atherosclerosis, pulmonary hypertension, and heart failure. The main site of hypoxic injury in the human body is the mitochondria, where oxygen acts as the final electron acceptor in the process of oxidative phosphorylation. Hypoxia-inducible factor (HIF) is activated in hypoxic conditions and acts as an important modulator of diverse target genes in the human body. The downstream genes of HIF include vital modulators of cardiovascular-related signaling pathways. Therefore, it is hypothesized that HIF represents a potential therapeutic target for the treatment and prevention of cardiovascular diseases. In this short review, we introduce the pathophysiology of hypoxic injury in cardiovascular disease, and we conclude from convincing evidence that HIF can modulate relevant cardioprotective signaling pathways.
Highlights
Oxygen is essential for most eukaryotic organisms to maintain normal cellular function and survival
Mitochondria generate reactive oxygen species (ROS) species, including superoxide and H2O2, from the leakage of electrons from the electron transport chain (ETC); this process contributes to cellular signaling and does not cause damage to the cell (McElroy and Chandel, 2017)
Mouse pulmonary hypertension model induced by hypoxia-induced mitogenic factor (HIMF) injection Mouse model by normoxia or chronic hypoxia (10% O2) for 30 days
Summary
Oxygen is essential for most eukaryotic organisms to maintain normal cellular function and survival. Hypoxia is usually synonymous with cellular dysfunction and it may lead to cell death under chronic circumstances (Sendoel and Hengartner, 2014) It is well-known that this condition is a major cause of several severe cardiovascular diseases (Han et al, 2014). HIF-1 in Hypoxia-Related Cardiovascular Diseases of target genes that can initiate distinct responses to low oxygen availability While these regulated gene signaling pathways are known to mediate protective pathways in the short term, they can eventually lead to cardiovascular dysfunction (Abe et al, 2017). In this short review, we highlight the importance of HIF-1 cellular hypoxia and the pathophysiology of cardiovascular disease, and we offer insight into potential clinical therapies involving the modulation of HIF-1 pathways. Before we turn to the role of HIF1 in cardiovascular disease, it is instructive to review the sequence of events leading to cellular dysfunction during hypoxia
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
