ZyVersa Therapeutics Announces a Publication in the Peer-Reviewed Journal, Aging, Linking Inflammasome NLRP3 Activation with Age-Related Structural Changes in the Kidney and Reduced Kidney Function

• Chronic kidney disease is most common in people 65 years and older.
  
• NLRP3 inflammasomes signaling in the kidneys’ filtration system (“glomerular podocytes”) occurs as early as middle age, leading to scarring, podocyte loss, and impaired function, which may be a critical contributor to a lower threshold for developing kidney disease in older people.
• Age-related inflammasome signaling and its effects are compounded in the presence of kidney disease, leading to poorer outcomes.
• 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., Oct. 18, 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, Aging, demonstrating that inflammasome NLRP3 activation is associated with an age-related decline in kidney health, which is compounded in the presence of kidney disease resulting in worsening outcomes.

In the paper titled, “Inhibiting NLRP3 signaling in aging podocytes improves their life-and health-span,” the authors conducted studies in various mouse models, human kidney tissues, and human kidney organoids. Data demonstrate a critical role for NLRP3 inflammasomes in age-related kidney deterioration, which is exacerbated in the presence of kidney disease. Following are key findings reported in the paper:

• Glomerular NLRP3 levels in human kidney tissue were associated with pathological changes in the kidneys’ filtration system: higher levels of glomerular scarring (glomerulosclerosis) and enlargement (hypertrophy), and reduced podocyte density.
• Glomerular NLRP3 inflammasome levels were higher in aged mice with experimental focal segmental glomerulosclerosis (FSGS) compared to age-matched mice without disease, indicating that FSGS injury augments the age-dependent increase of NLRP3 signaling.
• NLRP3 inflammasome signaling and its effects on podocytes may be a critical contributor to a lower threshold for developing kidney disease in older people.
• Reduction in NLRP3 signaling, either pharmacologically or by gene deletion, in human kidney organoids and in middle-aged mice decreased age-associated podocyte injury.

The authors stated, “By showing that in aged mice with experimental FSGS, injury augments the age-dependent increase of NLRP3 signaling, it makes this pathway an intriguing therapeutic target for podocyte (kidney) diseases in the elderly.” To read the article, Click Here.