ArticleImmunity, inflammation and disease2025
Mertk
Article in Immunity, inflammation and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The trial behind it
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Who cites it
4 citing papers in PubMed.
- Endothelial cell LGR4 maintains liver sinusoidal endothelial cell Identity and protects against hepatic steatosis.Life sciences · 2026Article
- Mitophagy in Metabolic Dysfunction-Associated Fatty Liver Disease: Mechanisms, Regulatory Networks, and Therapeutic Perspectives.Inflammation · 2026Review
- Nanotherapeutic strategy via ADSC-mitoEVs rescues ischaemic angiogenesis through mitophagy and mitochondrial metabolic reprogramming.Journal of nanobiotechnology · 2026Article
- MertkImmunity, inflammation and disease · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
backgroundMer tyrosine kinase (Mertk) regulating mitochondrial function of liver sinusoidal endothelial cells (LSECs) in metabolic dysfunction-associated steatohepatitis (MASH) remains unclear.
methodsMertk/p-Mertk, PINK1, and ERK/p-ERK expression in steatotic LSECs and livers of MASH mice were studied. Mitochondrial functions were assessed via immunofluorescence, Western blot, and qPCR. C-Kit
resultsOv-Mertk would markedly stimulate ERK, and ERK further suppress downstream PINK1. Higher levels of Mertk/p-Mertk and lower levels of PINK1 were confirmed in steatotic LSECs and MASH mice livers. Steatotic LSECs
conclusionMertk negatively regulates PINK1-mediated mitophagy in LSECs through the p-ERK signaling pathway, thereby accelerating MASH progression. Therefore, LSECs deficient of Mertk should be a novel therapy for reversing PINK1-related mitophagy and MASH.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.