Enhanced CHI3L1 promotes macrophage activation in persistent inflammatory events of ulcerative interstitial cystitis

Key Points

CHI3L1 enhances macrophage activation during persistent inflammatory events, contributing to chronic inflammation.
Key evidence shows increased glycolysis and MYC signaling linked to inflammation in interstitial cystitis.
Observational analysis highlights the role of CHI3L1 in reprogramming macrophage metabolism toward glycolysis.
These findings call for further exploration of CHI3L1 as a therapeutic target to disrupt inflammatory cycles.

Abstract

CHI3L1 exacerbates PIEs in HIC by reprogramming macrophage metabolism toward glycolysis and sustaining inflammation via MYC signaling. These findings establish CHI3L1 as a central regulator of chronic inflammation in HIC and highlight its potential as a therapeutic target for disrupting pathological immune-metabolic cycles.

Enhanced CHI3L1 promotes macrophage activation in persistent inflammatory events of ulcerative interstitial cystitis

Key Points

Abstract

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