ZyVersa Therapeutics Announces Article in Peer-Reviewed Journal, Ecotoxicology and Environmental Safety, Linking Air Pollution with Development and Progression of Chronic Kidney Disease That Can Be Attenuated by Inhibiting Inflammasome NLRP3 Activation

• Despite decades of effective environmental policy and improved air quality in the US, air pollution remains the greatest environmental health risk factor, contributing to 100,000 to 200,000 incremental deaths annually, primarily from fine particulate matter (PM_2.5) derived from pollutants including vehicle and industrial emissions from fuel and biomass combustion, cigarette smoke, volcanos, fires, and desert dust.
• PM_2.5 is inhaled into the lungs, spreading through the bloodstream to other organs, especially the kidney, which accumulates it during glomerular filtration, where it triggers NLRP3 inflammasome activation resulting in damaging inflammation and cell death (pyroptosis) leading to chronic kidney disease and its progression.
• ZyVersa is developing Inflammasome ASC Inhibitor IC 100 which can inhibit up to 12 different inflammasomes (including NLRP3 inflammasomes) and their associated ASC specks which perpetuate damaging inflammation.
  

WESTON, Fla., Nov. 06, 2023 (GLOBE NEWSWIRE) -- ZyVersa Therapeutics, Inc. (Nasdaq: ZVSA, or “ZyVersa”), a clinical stage specialty biopharmaceutical company developing first-in-class drugs for treatment of inflammatory and renal diseases, announces publication of an article in the peer-reviewed journal, Ecotoxicology and Environmental Safety, demonstrating that inhibiting NLRP3 inflammasomes can attenuate kidney damage and dysfunction associated with the environmental pollutant, PM_2.5.

In the paper titled, “PM_2.5 induces renal tubular injury by activating NLRP3-mediated pyroptosis,” the authors conducted studies in a mouse model exposed to high concentrations of ambient PM_2.5 for 12 weeks, and in a mouse kidney cell line. Following are key findings reported in the paper:

• PM_2.5 exposure leads to kidney structural changes and functional impairment.
• Inflammasome NLRP3-induced Inflammation and pyroptosis were increased in PM_2.5-exposed kidney tissues.
• Inhibiting the inflammasome NLRP3 pathway, including downstream caspase-1, rescued the kidneys from PM_2.5-induced cell death.
  

The authors stated, “We further provided evidence that NLRP3-mediated pyroptosis plays critical roles in the progression of kidney injury induced by PM_2.5 exposure. Inhibiting the activation of NLRP3 inflammasome can remarkably protect the renal tubular epithelial cells from PM_2.5-induced proptosis.” To read the article, Click Here.