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Genetic and pharmacologic modulations elucidate NRF2 protective role in acute pancreatitis

Year: 2026

Type: article

Abstract: Nonresolving inflammation is a major cause of acute pancreatitis (AP) mortality. Oxidative stress drives inflammation in various diseases, but its role in AP remains poorly understood, and targeted therapies are lacking. We show that acinar cell nuclear factor erythroid 2-related factor 2 (NRF2) activation in experimental AP was insufficient to prevent oxidative stress; however, additional NRF2 activation with sulforaphane markedly reduced oxidative stress, the inflammatory response, and disease severity. The results highlight pharmacologic NRF2 activators as a promising therapeutic approach for pancreatitis.

Source: American Journal of Physiology-Gastrointestinal and Liver Physiology

DOI: 10.1152/ajpgi.00032.2026

Authors: Olga A. Mareninova, Alex G. Chang, Sebastian Hernandez Malpica, Jerik A. Pineda, Rami Mamita, Natalia Shalbueva, Ilya Gukovsky, Anna S. Gukovskaya

Institutions: University of California, Los Angeles, VA Greater Los Angeles Healthcare System

Language: English

Topic: Pancreatitis Pathology and Treatment

Subfield: Surgery

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: hybrid

Funders: U.S. Department of Veterans Affairs, Biomedical Laboratory Research and Development, VA Office of Research and Development, National Institutes of Health, National Institute on Alcohol Abuse and Alcoholism, National Institute of Diabetes and Digestive and Kidney Diseases

Awards: G2387993214, Lysosomal Damage, Impaired Autophagy, and Alcoholic Pancreatitis, G3100142965, G3311510754, G6102332438, Dysregulated cholesterol homeostasis, caused by lysosomal/autophagy dysfunction, mediates pancreatitis, Southern California Research Center for ALPD and Cirrhosis, Impaired autophagy, mitochondrial dysfunction, and inflammation in pancreatitis

OpenAlex ID: W7171822957

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