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The production of hypochlorous acid (HClO) is well recognized as a biomarker for liver injury, however, existing HClO bioimaging probes often lack specificity. Inspired by the specific recognition of oxime and hydrazide groups for HClO, we developed a novel N-alkyhydrazone moiety as a recognition unit for HClO. This moiety was integrated into an iridium(III) complex, creating a mitochondria-targeted luminescence probe for HClO that leverages the lipophilicity and cationic characteristics of iridium(III) complexes. The probe offers advantages including high specificity over other reactive oxygen species (ROS), rapid response of within 5 min, as well as robust stability. Furthermore, it effectively images both endogenous and endogenous mitochondrial HClO in liver injury-modeled cells and demonstrates excellent penetration capabilities in 3D cell spheres, highlighting its potential for diagnosing liver injury.
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http://dx.doi.org/10.1016/j.aca.2025.344327 | DOI Listing |
Ren Fail
December 2025
Department of Critical Care Medicine, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, China.
This study aimed to develop a predictive model and construct a graded nomogram to estimate the risk of severe acute kidney injury (AKI) in patients without preexisting kidney dysfunction undergoing liver transplantation (LT). Patients undergoing LT between January 2022 and June 2023 were prospectively screened. Severe AKI was defined as Kidney Disease: Improving Global Outcomes stage 3.
View Article and Find Full Text PDFTrends Mol Med
September 2025
Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address:
Ferroptosis, a regulated cell death pathway driven by iron-catalyzed lipid peroxidation, has recently been implicated as a major cause of hepatic injury in metabolic dysfunction-associated fatty liver disease (MAFLD). This review highlights how the identification of hyperoxidized peroxiredoxin 3 (PRDX3) as a ferroptosis-specific marker has led to the discovery that ferroptosis contributes to liver injury in MAFLD, and summarizes other emerging evidence connecting ferroptosis to MAFLD pathogenesis. These new findings suggest that dietary fat composition and genetic variants such as PNPLA3(I148M) may affect the progression of MAFLD by regulating cellular sensitivity to ferroptosis.
View Article and Find Full Text PDFIntern Med
September 2025
Division of Nephrology, Department of Internal Medicine, Jichi Medical University, Japan.
Intern Med
September 2025
Fujita Health University School of Medicine, Department of Nephrology, Japan.
An 81-year-old man was treated with prednisolone, avacopan, and rituximab for microscopic polyangiitis and sulfamethoxazole/trimethoprim (SMX/TMP) and vonoprazan for prophylaxis. The liver enzyme levels were elevated 42 days after avacopan administration. Avacopan, SMX/TMP, and vonoprazan treatment were discontinued.
View Article and Find Full Text PDFFree Radic Biol Med
September 2025
Center of Infectious Diseases, West China Hospital, Sichuan University, Chengdu, China. Electronic address:
Metabolic dysfunction-associated steatotic liver disease (MASLD), a leading cause of chronic liver pathology, lacks effective therapies. This study identifies ferroptosis-a lipid peroxidation-driven, iron-dependent form of cell death-as a central pathogenic mechanism in MASLD. Integrative proteomic and histopathological analyses of human and murine MASLD livers revealed marked ferroptosis activation, characterized by dysregulated iron metabolism (reduced FTH1 and GPX4; elevated ACSL4) and oxidative stress.
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