Endogenously generated arachidonate‐derived ligands for TRPV1 induce cardiac protection in sepsis

What is it about?

Sepsis occurs in response to blood infections and at its worst causes organ failure, with disturbed heart function particularly predicting death in patients. Treatment includes early administration of antibiotics, however this is inadequate in patients with progressed sepsis. We have shown that activation of a protein called transient receptor-potential vanilloid receptor type-1 (TRPV1) expressed on specialized nerves in the heart plays a role in limiting the damaging effects of sepsis on the heart. In addition, we show that during sepsis neuronal TRPV1 in the heart is activated by 20-HETE (a potent activator of TRPV1 made in the body during sepsis). Upon activation, the neurons release a mediator called CGRP into the surrounding tissue and this CGRP then protects the heart against the damage caused by systemic infection. Importantly, giving more CGRP provides even greater protection thus identifying a 20-HETE-TRPV1-CGRP signalling pathway as a potential drug target for patients with sepsis.

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