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| http://dx.doi.org/10.26599/1671-5411.2024.02.007 | DOI Listing |
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sVEGFR3 alleviates myocardial ischemia/reperfusion injury through regulating mitochondrial homeostasis and immune cell infiltration.
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Department of Cardiac Surgery, First Affiliated Hospital of Sun Yat-sen University, 58 Zhongshan II Rd, Guangzhou, 510080, China.
Recent studies have suggested that sVEGFR3 is involved in cardiac diseases by regulating lymphangiogenesis; however, results are inconsistent. The aim of this study was to investigate the function and mechanism of sVEGFR3 in myocardial ischemia/reperfusion injury (MI/RI). sVEGFR3 effects were evaluated in vivo in mice subjected to MI/RI, and in vitro using HL-1 cells exposed to oxygen-glucose deprivation/reperfusion.
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Metabolic rewiring underlies effective macrophages defense to respond disease microenvironment. However, the underlying mechanisms driving metabolic rewiring to enhance macrophage effector functions remain unclear. Here, we demonstrated that the metabolic reprogramming in inflammatory macrophages depended on the acetylation of CLYBL, a citramalyl-CoA lyase, at lysine 154 (K154), and blocking CLYBL-K154 acetylation restricted the release of pro-inflammatory factors.
View Article and Find Full Text PDFInhibition of Endothelial-Mesenchymal Transition Mediated by Activin Receptor Type IIA Attenuates Valvular Injury Induced by Group A Streptococcus in Lewis Rats.
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View Article and Find Full Text PDFAstragali Radix-Notoginseng Radix et Rhizoma medicine pair prevents cardiac remodeling by improving mitochondrial dynamic balance.
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Astragali Radix (AR) and Notoginseng Radix et Rhizoma (NR) are frequently employed in cardiovascular disease treatment. However, the efficacy of the AR-NR medicine pair (AN) in improving cardiac remodeling and its underlying mechanism remains unclear. This study aimed to evaluate AN's cardioprotective effect and potential mechanism on cardiac remodeling using transverse aortic constriction (TAC) in mice and angiotensin II (Ang II)-induced neonatal rat cardiomyocytes (NRCMs) and fibroblasts in vitro.
View Article and Find Full Text PDFLutein, a non-provitamin A carotenoid, reduces cisplatin-induced cardiotoxicity.
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Department of Pharmacology, Vocational School of Health Services, Adıyaman University, Adıyaman, Turkey. Electronic address:
Cardiovascular complications resulting from cisplatin (CS) are a significant factor that can disrupt the treatment plan associated with this chemotherapy. This information led us to investigate the effectiveness of lutein (LT), which has antioxidant effects, in preventing CS-induced cardiotoxic effects. After 28 rats were randomly divided into four equal groups, saline (1ml/day) was administered to the control group, LT (100mg/kg/day) to the LT group, CS (10mg/kg) to the CS group, and active agents in the LT and CS groups were administered to the CS + LT group in the same dose and manner.
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