Sepsis is a state of infection with serious systemic manifestations, and if severe enough, can be
associated with multiple organ dysfunction and systemic hypotension, which can cause tissues to be hypoxic.
Inflammation, as part of the multifaceted biological response to injurious stimuli, such as pathogens or
damaged tissues and cells, underlies these biological processes. Prolonged and persistent inflammation, also
known as chronic inflammation, results in progressive alteration in the various types of cells at the site of
inflammation and is characterized by the simultaneous destruction and healing of tissue during the process.
Tissue hypoxia during inflammation is not just a simple bystander process, but can considerably affect the development or
attenuation of inflammation by causing the regulation of hypoxia-dependent gene expression. Indeed, the study of
transcriptionally regulated tissue adaptation to hypoxia requires intense investigation to help control hypoxia-induced
inflammation and organ failure. In this review, I have described the pathophysiology of sepsis with respect to oxygen
metabolism and expression of hypoxia-inducible factor 1.
Keywords: Chemokine, cytokine, hypoxia, hypoxia-inducible factor, inflammation, NF-κB, sepsis.
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