As the most severe manifestation of coronary artery disease, myocardial infarction (MI) is a complex and multifactorial pathophysiologic process. However, the pathogenesis that underlies MI remains unclear. Here, we generated a MI mouse model by ligation of the proximal left anterior descending coronary artery. The transcriptome and proteome, at different time points after MI, were detected and analysed. Immune-related pathways, cell cycle-related pathways, and extracellular matrix remodelling-related pathways were significantly increased after MI. Not only innate immune cells but also adaptive immune cells participated in the early stage of MI. Proteins that functioned in blood agglutination, fibrinolysis, secretion, and immunity were significantly changed after MI. Nppa, Serpina3n, and Anxa1, three secreted proteins that can easily be detected in blood, were significantly changed after MI. Our discoveries not only reveal the molecular and cellular changes in MI but also identify potential candidate biomarkers of MI for clinical diagnosis or treatment.
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http://dx.doi.org/10.1038/s41420-019-0152-z | DOI Listing |
Environ Pollut
January 2025
College of Energy Environment and Safety Engineering, China Jiliang University, Hangzhou, Zhejiang, 310016, PR China. Electronic address:
The extensive presence of per-/polyfluoroalkyl substances (PFASs) in the environment and their adverse effects on organisms have garnered increasing concern. With the shift of industrial development from legacy to emerging PFASs, expanding the understanding of molecular responses to legacy and emerging PFASs is essential to accurately assess their risks to organisms. Compared with traditional toxicological approaches, omics technologies including transcriptomics, proteomics, metabolomics/lipidomics, and microbiomics allow comprehensive analysis of the molecular changes that occur in organisms after PFAS exposure.
View Article and Find Full Text PDFAgeing Res Rev
January 2025
Department of Cardiovascular Center, TheFirst Hospital of Jilin University, Changchun,Jilin, China.
Sirtuin-3 (SIRT3) in mitochondria has nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase activity. As such, SIRT3 is crucial in cardiovascular and neurodegenerative diseases. Advanced proteomics and transcriptomics studies have revealed that SIRT3 expression becomes altered when the heart or brain is affected by external stimuli or disease, such as diabetic cardiomyopathy, atherosclerosis, myocardial infarction, Alzheimer's disease, Huntington's disease, and Parkinson's disease.
View Article and Find Full Text PDFJ Hepatol
January 2025
Centre for Regenerative Medicine, Institute for Regeneration and Repair, University of Edinburgh, Edinburgh, EH16 4UU, United Kingdom. Electronic address:
Background & Aims: Hepatocyte transplantation has shown promise for genetic diseases of the hepatocytes but to date has shown limited efficacy for non-genetic forms of severe liver injury. Limited cell engraftment and poor function of donor hepatocytes in recipient livers impacts the clinical utility of hepatocyte cell therapy. The mechanisms underpinning this are poorly understood.
View Article and Find Full Text PDFComp Biochem Physiol Part D Genomics Proteomics
December 2024
Key Laboratory of Plant Genetics and Molecular Breeding, Zhoukou Normal University, Zhoukou 466001, China; Henan Key Laboratory of Crop Molecular Breeding & Bioreactor, Zhoukou 466001, China. Electronic address:
Uridine diphosphate-glycosyltransferases (UGTs) are responsible for glycosylation by combining various small lipophilic molecules with sugars to produce water-soluble glycosides, which are crucial for the metabolism of plant secondary metabolites and detoxification in insects. This study presents a genome-wide analysis of the UGT gene family in the brown planthopper, Nilaparvata lugens, a destructive insect pest of rice in Asia. Based on the similarity to UGT homologs from other organisms, 20 putative NlUGT genes were identified in N.
View Article and Find Full Text PDFBackground: Axial Spondyloarthritis (axSpA) is a chronic inflammatory rheumatic condition affecting the axial skeleton, leading to pain, stiffness, and fatigue. While biologic therapies have improved clinical management, many patients experience partial or no responses, resulting in delays in disease control. Additionally, the risk of adverse events and increased costs remains a concern.
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