Pulmonary hypertension (PH) is marked by elevated mean pulmonary
arterial pressure, unfavorable vascular remodeling and right ventricular failure. Current
enormous amounts of clinical and preclinical data suggest the role of inflammation as a
crucial factor for PH onset and development by modulating both innate and adaptive
immune responses. In this context, NLRP3 inflammasome appears as a key step in the
signaling cascade that negatively regulates various PH-associated conditions by
inducing inflammatory outbursts. The activation of NLRP3 by pathogen-associated
molecular pattern molecules/damage-associated molecular pattern molecules and
caspase-1 mediated release of proinflammatory cytokines IL-1β and IL-18 are the key
molecular events associated with NLRP3 inflammasomal pathway. Released IL-1β and
IL-18 bring about adverse consequences on the pulmonary vasculature and the
resulting onset of PH. Within this section, we will provide an in-depth understanding of
present pulmonary hypertension (PH) treatments and their shortcomings. We will also
discuss the contribution of NLRP3 inflammasomes in promoting inflammation within
the context of PH pathobiology, as well as explore potential therapeutic approaches to
target them.
Keywords: Inflammasome, Interleukin, Lung, NLRP3, Pulmonary hypertension.
