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Turn Up the HETE on Septic Shock.

Kirby Thomas¹, Luke Strong, Fan Fan

¹Department of Pharmacology, University of Mississippi Medical Center, Jackson, MS.

Journal of Cardiovascular Pharmacology

|May 16, 2022

Summary

In septic shock, inhibiting vascular 20-hydroxyeicosatetraenoic acid (20-HETE) contributes to organ failure. A new study shows a 20-HETE mimetic prevents septic shock symptoms in rats, suggesting potential clinical trials.

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Area of Science:

Cardiovascular Pharmacology
Sepsis Pathophysiology
Vascular Biology

Background:

Septic shock causes organ dysfunction and death due to dysregulated inflammatory responses to infection.
Current treatments for septic shock are primarily supportive, lacking specific pharmacologic interventions.
Vascular 20-hydroxyeicosatetraenoic acid (20-HETE) inhibition by nitric oxide is implicated in sepsis pathogenesis.

Purpose of the Study:

To review evidence on the role of vascular 20-HETE in sepsis.
To highlight findings on a 20-HETE mimetic's effects on septic shock models.
To advocate for clinical trials of 20-HETE mimetics in septic shock.

Main Methods:

Review of existing literature on 20-HETE and nitric oxide in sepsis.
Analysis of a study using a 20-HETE mimetic in lipopolysaccharide-induced sepsis in rats.
Examination of the GPR75/20-HETE receptor pathway.

Main Results:

Inhibition of vascular 20-HETE by nitric oxide is a key factor in sepsis.
Administration of a 20-HETE mimetic prevented vascular hyporeactivity, hypotension, and tachycardia in rats.
The protective effects were mediated by activation of the GPR75/20-HETE receptor.

Conclusions:

Vascular 20-HETE plays a critical role in the pathophysiology of septic shock.
Targeting the GPR75/20-HETE receptor with mimetics shows promise for treating septic shock.
Clinical trials investigating 20-HETE mimetics are warranted to prevent hypotension, organ failure, and mortality in septic shock.