This study aimed at measuring the influence of a low salt diet on the development of experimental atherosclerosis in moderately hyperlipidemic mice. Experiments were carried out on LDL receptor (LDLR) knockout (KO) mice, or apolipoprotein E (apoE) KO mice on a low sodium chloride diet (LSD) as compared with a normal salt diet (NSD). On LSD, the rise of the plasma concentrations of TG and nonesterified fatty acid (NEFA) was, respectively, 19% and 34% in LDLR KO mice, and 21% and 35% in apoE KO mice, and that of plasma cholesterol was limited to the LDLR KO group alone (15%). Probably due to the apoE KO severe hypercholesterolemia, the arterial inner-wall fat storage was not influenced by the diet salt content and was far more abundant in the apoE KO than in the LDLR KO mice. However, in the less severe hypercholesterolemia of the LDLR KO mice, lipid deposits on the LSD were greater than on the NSD. Arterial fat storage correlated with NEFA concentrations in the LDLR KO mice alone (n = 14, P = 0.0065). Thus, dietary sodium chloride restriction enhances aortic wall lipid storage in moderately hyperlipidemic mice.
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http://dx.doi.org/10.1194/jlr.M200330-JLR200 | DOI Listing |
Front Pharmacol
January 2025
Human Molecular Genetics Research Unit, Institute of Molecular Biology and Biotechnology, Faculty of Biology, Adam Mickiewicz University, Poznan, Poland.
Cardiovascular diseases (CVDs) include atherosclerosis, which is an inflammatory disease of large and medium vessels that leads to atherosclerotic plaque formation. The key factors contributing to the onset and progression of atherosclerosis include the pro-inflammatory cytokines interferon (IFN)α and IFNγ and the pattern recognition receptor (PRR) Toll-like receptor 4 (TLR4). Together, they trigger the activation of IFN regulatory factors (IRFs) and signal transducer and activator of transcription (STAT)s.
View Article and Find Full Text PDFDiabetes Obes Metab
January 2025
The Second Affiliated Hospital, Zhengzhou University, Zhengzhou, China.
Background: Proprotein convertase subtilisin/kexin type 9 (PCSK9) is mainly secreted by the liver, and plays a crucial role in lipid metabolism disorder. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) can regulate lipid metabolism through various pathways, including reducing visceral fat accumulation, modulating serum lipoprotein levels and alleviating hepatic steatosis. However, the specific regulatory mechanisms remain unclear.
View Article and Find Full Text PDFEMBO J
January 2025
Department of Pharmacology, School of Pharmacy, China Pharmaceutical University, Nanjing, Jiangsu, 210009, China.
Metabolic requirements of dividing hepatocytes are prerequisite for liver regeneration after injury. In contrast to transcriptional dynamics during liver repair, its metabolic dependencies remain poorly defined. Here, we screened metabolic genes differentially regulated during liver regeneration, and report that SLC13A2, a transporter for TCA cycle intermediates, is decreased in rapid response to partial hepatectomy in mice and recovered along restoration of liver mass and function.
View Article and Find Full Text PDFLife Sci
January 2025
Department of Laboratory Medicine, Guangdong Provincial Key Laboratory of Precision Medical Diagnostics, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. Electronic address:
The dysfunction of the endothelial lining in lesion-prone areas of the arterial vasculature significantly contributes to the pathobiology of atherosclerotic cardiovascular disease. Recent studies suggested that UDP-glucose pyrophosphorylase 2 (UGP2) plays a role in cell proliferation and survival. This study investigates the anti-apoptotic and anti-atherogenic effects of UGP2 both in vitro and in vivo.
View Article and Find Full Text PDFJ Cardiovasc Transl Res
January 2025
Department of Vascular and Endovascular Surgery, Changzheng Hospital, Affiliated to the Naval Medical University, Shanghai, 200003, China.
CHI3L1 is strongly associated with atherosclerosis, but its role in macrophages remains unknown. In this study, we observed a significant up-regulation of CHI3L1 in both carotid plaques and serum of symptomatic patients, and demonstrated that CHI3L1 impairs the efferocytosis of macrophages by down-regulating crucial efferocytic mediator MFGE8 through inhibiting ATF2, which binds directly to the enhancer of MFGE8. In human plaques, we observed a negative correlation between CHI3L1 expression and both ATF2 and MFGE8 levels, further proved their involvement in plaque destabilization.
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