Inflammasome Activation in Pulmonary Arterial Hypertension

Anna Foley; Benjamin E Steinberg; Neil M Goldenberg

doi:10.3389/fmed.2021.826557

Inflammasome Activation in Pulmonary Arterial Hypertension

Front Med (Lausanne). 2022 Jan 13:8:826557. doi: 10.3389/fmed.2021.826557. eCollection 2021.

Authors

Anna Foley¹, Benjamin E Steinberg^{1

2}, Neil M Goldenberg^{1

2}

Affiliations

¹ Department of Physiology, University of Toronto, Toronto, ON, Canada.
² Department of Anesthesia and Pain Medicine, The Hospital for Sick Children, The University of Toronto, Toronto, ON, Canada.

Abstract

Inflammasomes are multi-protein complexes that sense both infectious and sterile inflammatory stimuli, launching a cascade of responses to propagate danger signaling throughout an affected tissue. Recent studies have implicated inflammasome activation in a variety of pulmonary diseases, including pulmonary arterial hypertension (PAH). Indeed, the end-products of inflammasome activation, including interleukin (IL)-1β, IL-18, and lytic cell death ("pyroptosis") are all key biomarkers of PAH, and are potentially therapeutic targets for human disease. This review summarizes current knowledge of inflammasome activation in immune and vascular cells of the lung, with a focus on the role of these pathways in the pathogenesis of PAH. Special emphasis is placed on areas of potential drug development focused on inhibition of inflammasomes and their downstream effectors.

Keywords: endothelial; inflammasome; macrophage; pulmonary hypertension; vascular remodeling.

Publication types

Review