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http://dx.doi.org/10.1038/onc.2015.322 | DOI Listing |
Invest Ophthalmol Vis Sci
December 2024
Department of Ophthalmology, Eugene and Marilyn Glick Eye Institute, Indiana University School of Medicine, Indianapolis, Indiana, United States.
Purpose: Alport syndrome (AS) is a genetic condition caused by a dysfunctional collagen (IV) α3α4α5 heterotrimer, leading to basement membrane instability and, ultimately, abnormalities in the kidney, inner ear, and eyes. This study aimed to characterize ocular pathology of AS by focusing on inflammatory and fibrotic markers.
Methods: Col4a3tm1Dec knockout (KO) mice eyes were evaluated for the localization of collagen (IV) α3 and collagen (IV) α4, then stained for transforming growth factor-β1 (TGF-β1), TGF-β2, connective tissue growth factor (CTGF), and β-catenin.
FEBS J
January 2025
Department of Neurosurgery, General Hospital of the Northern Theater Command, Shenyang, China.
Atherosclerosis (AS) is a vascular disease associated with endothelial damage, plaque formation, and retinal neovascularization (RNV), leading to visual impairment. Research indicates that vascular endothelial dysfunction, lipid deposition, and inflammatory responses contribute to the formation of plaques and atherosclerotic lesions. Among the common complications, studies have shown that RNV and the molecular mechanisms of AS hold significant clinical importance.
View Article and Find Full Text PDFInt J Mol Sci
September 2024
Department of Molecular Biology & Genetics, School of Health Sciences, Democritus University of Thrace, 68100 Alexandroupolis, Greece.
Aldehyde dehydrogenases (ALDHs) constitute a diverse superfamily of NAD(P)-dependent enzymes pivotal in oxidizing endogenous and exogenous aldehydes to carboxylic acids. Beyond metabolic roles, ALDHs participate in essential biological processes, including differentiation, embryogenesis and the DNA damage response, while also serving as markers for cancer stem cells (CSCs). Aldehyde dehydrogenase 1B1 (ALDH1B1) is a mitochondrial enzyme involved in the detoxification of lipid peroxidation by-products and metabolism of various aldehyde substrates.
View Article and Find Full Text PDFJ Transl Med
October 2024
Department of General Surgery, Second Affiliated Hospital of Nanchang University, Nanchang, 330000, China.
J Biol Chem
November 2024
Department of Biochemistry and Molecular Biology, SUNY Upstate Medical University, Syracuse, New York, United States. Electronic address:
Our understanding of acute leukemia pathology is heavily dependent on 11q23 chromosomal translocations involving the mixed lineage leukemia-1 (MLL1) gene, a key player in histone H3 lysine 4 (H3K4) methylation. These translocations result in MLL1-fusion (MLL1) proteins that are thought to drive leukemogenesis. However, the mechanism behind increased H3K4 trimethylation in MLL1-leukemic stem cells (MLL1-LSCs), following loss of the catalytic SET domain of MLL1 (known for H3K4 monomethylation and dimethylation) remains unclear.
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