Abstract
Physiology A challenge in treating the systemic inflammation that occurs in sepsis is the increase in endothelial permeability that leads to widespread tissue edema and immune cell infiltration. Maier-Begandt et al. uncovered a pathway activated specifically in veins by tumor necrosis factor–α (TNFα), a proinflammatory cytokine whose circulating levels increase greatly during sepsis. TNFα treatment resulted in the activation of Pannexin 1 channels, which ultimately led to disrupted tight junctions in veins but not in arteries. Sepsis induced less lung edema and was less fatal to Pannexin 1–deficient mice compared with control mice. Sci. Signal. 14 , eaba2940 (2021).
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