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Background: Hepatic regeneration requires coordinated signal transduction for efficient restoration of functional liver mass. This study sought to determine changes in lysophosphatidic acid (LPA) and LPA receptor (LPAR) 1-6 expression in regenerating liver following two-thirds partial hepatectomy (PHx).
Methods: Liver tissue and blood were collected from male C57BL/6 mice following PHx. Circulating LPA was measured by enzyme-linked immunosorbent assay (ELISA) and hepatic LPAR mRNA and protein expression were determined.
Results: Circulating LPA increased 72 h after PHx and remained significantly elevated for up to 7 days post-PHx. Analysis of LPAR expression after PHx demonstrated significant increases in LPAR1, LPAR3 and LPAR6 mRNA and protein in a time-dependent manner for up to 7 days post-PHx. Conversely, LPAR2, LPAR4 and LPAR5 mRNA were barely detected in normal liver and did not significantly change after PHx. Changes in LPAR1 expression were confined to non-parenchymal cells following PHx.
Conclusions: Liver regeneration following PHx is associated with significant changes in circulating LPA and hepatic LPAR1, LPAR3 and LPAR6 expression in a time- and cell-dependent manner. Furthermore, changes in LPA-LPAR post-PHx occur after the first round of hepatocyte division is complete.
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http://dx.doi.org/10.1111/hpb.12176 | DOI Listing |
Int J Mol Sci
August 2025
V.I. Kulakov National Medical Research Center for Obstetrics Gynecology and Perinatology, Ministry of Healthcare of Russian Federation, 117997 Moscow, Russia.
The maternal circulating proteome reflects critical physiological adaptations during pregnancy, yet standardized reference profiles for early gestation are lacking. In this prospective study, we employed targeted liquid chromatography-multiple reaction monitoring-mass spectrometry (LC-MRM-MS) with stable isotope-labeled (SIS) standards to characterize the serum proteome of 83 women with uncomplicated singleton pregnancies between 11 and 13 weeks' gestation. Robust analysis quantified 115 proteins (83% of targets), with 101 meeting ICH M10 standards.
View Article and Find Full Text PDFBiomedicines
July 2025
Department of Biochemistry, Pomeranian Medical University, Powstańców Wielkopolskich 72, 70-111 Szczecin, Poland.
TGF-β is an immunosuppressive cytokine. Its signaling pathway plays a role in anti-inflammatory responses. Coronary artery disease (CAD) is a clinical consequence of atherosclerosis, which manifests as chronic inflammation and involves platelet mediators, including TGF-β.
View Article and Find Full Text PDFClin Ther
August 2025
Amgen, Inc., 1 Amgen Center Drive, Thousand Oaks, California.
Introduction: Cardiovascular disease (CVD) remains a major cause of premature mortality and disability worldwide, with China ranking among the highest in CVD deaths. Lipoprotein(a) (Lp(a)) is a circulating lipoprotein particle that, when elevated, may increase CVD risk. Reduced Lp(a) levels with existing cardiovascular treatments are modest, and evidence confirming whether lowering Lp(a) leads to cardiovascular benefit is lacking.
View Article and Find Full Text PDFThromb Haemost
August 2025
Thrombosis Research Group, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States.
Lipoprotein(a) [Lp(a)] is a circulating plasma lipoprotein with structural similarities to low-density lipoprotein (LDL), distinguished by the addition of apolipoprotein(a) to the LDL structure. Lp(a) levels are approximately 80% genetically determined, and distinct components of this complex particle are thought to confer atherogenic, inflammatory, and antifibrinolytic properties contributing to cardiovascular risk. A growing body of evidence has shown a causal association between elevated Lp(a) levels and both atherosclerotic cardiovascular disease (ASCVD) and valvular aortic stenosis.
View Article and Find Full Text PDFSci Rep
August 2025
Central Laboratory, Guiyang Maternal and Child Care Hospital, Guiyang, 550000, Guizhou, China.
Calcific aortic valve stenosis (CAVS) is steadily rising worldwide with no effective pharmacological agents available. Observational studies implicated dyslipidaemia as a risk factor for CAVS. Whether dyslipidaemia is causative for CAVS and the therapeutic potential of different lipid-modifying drug targets for CAVS treatment remains unclear.
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