Deletion of CD38 mitigates the severity of NEC in experimental settings by modulating macrophage-mediated inflammation.

ABSTRACT: Necrotizing enterocolitis (NEC) is a form of potentially lethal gastrointestinal inflammation that primarily affects preterm neonates. It is crucial to recognize that, while the disease carries significant risks, timely and effective medical intervention can greatly enhance the chances of survival. Additionally, NEC is closely linked to the activation of macrophages, highlighting the complex interplay between the immune response and disease progression. CD38, acting as an ectoenzyme, catalyzes the hydrolysis of NAD⁺ to produce cyclic ADP-ribose (cADPR), a reaction critical for modulating cellular redox balance and energy homeostasis. This enzymatic activity is particularly pertinent in the context of necrotizing enterocolitis (NEC). In this research, we investigated whether CD38

SUBMITTER: Ma Y 

PROVIDER: S-EPMC11489332 | biostudies-literature | 2024 Sep

REPOSITORIES: biostudies-literature