108 results match your criteria: "Shenzhen Sun Yat-Sen Cardiovascular Hospital[Affiliation]"

FSTL1 protects against acute aortic dissection by suppressing vascular smooth muscle cell phenotypic switching and degradation of the extracellular matrix.

J Mol Cell Cardiol

December 2024

Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510120, China; Department of Cardiology, Guangdong Provincial Key Laboratory of Arrhythmia and Electrophysiology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, Guangdong 510120, China. Electronic address:

Article Synopsis
  • Acute aortic dissection (AAD) is a serious cardiovascular emergency linked to changes in vascular smooth muscle cells and the breakdown of the extracellular matrix, with Follistatin-like 1 (FSTL1) found to play a protective role in related cardiovascular issues.
  • The study showed that FSTL1 levels were significantly lower in both human and mouse AAD models, and adding FSTL1 back helped improve VSMC function and reduce damage in the aorta.
  • Mechanistically, the research revealed that FSTL1 can enhance the phosphorylation of AMPK, suggesting that targeting FSTL1 could be a novel approach for preventing and treating AAD.
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The malfunction of endothelial progenitor cells (EPCs) due to ox-LDL is a risk contributor for arteriosclerotic disease. Meanwhile, lycopene possesses anti-inflammatory and antioxidative qualities. This investigation aimed to determine if lycopene can protect EPCs from ox-LDL-induced damage and to elucidate the underlying mechanism.

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Background: Carthamus tinctorius L., a traditional herbal medicine used for atherosclerosis (AS), lacks a clear understanding of its therapeutic mechanisms. This study aimed to investigate the therapeutic effects and mechanisms of Carthamus tinctorius L.

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Background: This study investigated whether gCTRP9 (globular C1q/tumor necrosis factor-related protein-9) could restore high-glucose (HG)-suppressed endothelial progenitor cell (EPC) functions by activating the endothelial nitric oxide synthase (eNOS).

Methods And Results: EPCs were treated with HG (25 mmol/L) and gCTRP9. Migration, adhesion, and tube formation assays were performed.

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This study investigated the protective effect of dapagliflozin on H9c2 cardiomyocyte function under high glucose and hypoxia/reoxygenation (HG-H/R) conditions and identified the underlying molecular mechanisms. Dapagliflozin reduced the level of lactate dehydrogenase and reactive oxygen species in cardiomyocytes under HG-H/R conditions and was accompanied by a decrease in caspase-3/9 activity. In addition, Dapagliflozin significantly reduced mitochondrial permeability transition pore opening and increased ATP content, accompanied by upregulation of OPA1 with autophagy-related protein molecules and activation of the AMPK/mTOR signalling pathway in HG-H/R treated cardiomyocytes.

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Dexmedetomidine might reduce delirium after cardiac surgery. We allocated 326 participants to an infusion of dexmedetomidine at a rate of 0.6 μg kg for 10 min and then at 0.

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Due to the complicated pathophysiology of cardiac hypertrophy, there are no effective therapies for the treatment of pathological cardiac hypertrophy. Accumulating evidence has demonstrated that circRNAs participate in the pathophysiology of cardiac hypertrophy. In this study, we investigated the regulatory mechanisms of the novel circ_0018553 in angiotensin II (Ang II)-induced cardiac hypertrophy.

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Ischemic postconditioning (IPost) represents short periods of nonlethal ischemia-reperfusion performed at the onset of reperfusion. Studies have shown that IPost involves various biological processes such as cell proliferation, apoptosis, and pyroptosis and can activate complex signaling pathways. CCL12 is a critical mediator in the inflammatory process after tissue injury.

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Inflammatory immune response is apparently one of the determinants of progressive exacerbation of valvular atrial fibrillation(VAF). Ferroptosis, an iron-dependent modality of regulated cell death, is involved in the immune regulation of cardiovascular disease. However, the relevant regulatory mechanisms of immune infiltration and ferroptosis in VAF have been less studied.

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Background: Acute kidney injury (AKI) is a common postoperative complication in pediatric patients undergoing cardiac surgery and associated with poor outcomes. Dexmedetomidine has the pharmacological features of organ protection in cardiac surgery patients. The aim of this meta-analysis is to investigate the effect of dexmedetomidine infusion on the incidence of AKI after cardiac surgery in pediatric patients.

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Background And Hypothesis: Glycemic variability in one fact that explain the differences in cardiovascular outcomes. The short-term fasting plasma glucose (FPG) variability may have an on major adverse cardiovascular events (MACE) in type 2 diabetes mellitus (T2DM) patients with ST-segment elevation myocardial infarction (STEMI).

Methods: This study retrospectively analyzed T2DM patients who underwent emergent percutaneous coronary intervention (PCI) due to STEMI in Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen, between January 2016 and March 2020.

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Background: A risk assessment of in-stent restenosis (ISR) patients is critical for providing adequate treatment. Nevertheless, the prognostic value of high-sensitivity CRP (hs-CRP) levels on ISR has not been consistently demonstrated in clinical studies. In the current meta-analysis, we aim to assess the predictive role of hs-CRP in patients treated with stenting.

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Exosomes of different origins have been found to be protective against ischemic-induced myocardial injury. This study examined the protective effects of circulating exosomes in the mice model of acute myocardial infarction (AMI) and explored the underlying molecular mechanisms. The effects of exosomes on myocardial injury were assessed in the AMI mice model.

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Background: The present study aims to explore risk factors related to in-stent restenosis (ISR) in elderly patients with coronary heart disease and type 2 diabetes within 2 years after the first drug-eluting stent (DES) implantation.

Methods: This case-control study retrospectively analyzed the clinical data of patients with coronary heart disease and diabetes undergoing percutaneous coronary intervention (PCI) in Shenzhen Sun Yat-sen Cardiovascular Hospital between January 2010 and March 2020. Univariate and multivariate models were used to assess independent factors for DES-ISR.

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Fluid Shear Stress Ameliorates Prehypertension-Associated Decline in Endothelium-Reparative Potential of Early Endothelial Progenitor Cells.

J Cardiovasc Transl Res

October 2022

Department of Cardiology, The Guangzhou Eighth People's Hospital, Guangzhou Medical University, NO.8 Huaying road, Baiyun district, Guangzhou city, 510000, Guangdong, China.

This study investigated the effects of prehypertension and shear stress on the reendothelialization potential of human early EPCs and explored its potential mechanisms. Early EPCs from the prehypertensive patients showed reduced migration and adhesion in vitro and demonstrated a significantly impaired in vivo reendothelialization capacity. Shear stress pretreatment markedly promoted the in vivo reendothelialization capacity of EPCs.

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Background: Percutaneous transluminal coronary angioplasty (PTCA) represents an efficient therapeutic method for atherosclerosis but conveys a risk of causing restenosis. Endothelial colony-forming cell-derived exosomes (ECFC-exosomes) are important mediators during vascular repair. This study aimed to investigate the therapeutic effects of ECFC-exosomes in a rat model of atherosclerosis and to explore the molecular mechanisms underlying the ECFC-exosome-mediated effects on ox-LDL-induced endothelial injury.

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Exogenous HS reverses high glucose-induced endothelial progenitor cells dysfunction via regulating autophagy.

Bioengineered

January 2022

Department of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen, (Shenzhen Sun Yat-sen Cardiovascular Hospital), Shenzhen, China.

This study aims to determine the effect of exogenous hydrogen sulfide (HS) under high glucose (HG)-induced injury in endothelial progenitor cells (EPCs), and to explore the possible underlying mechanisms. Mononuclear cells were isolated from the peripheral blood of healthy volunteers by density-gradient centrifugation and identified as late EPCs by immunofluorescence and flow cytometry. EPCs were treated with high concentrations of glucose, HS, Baf-A1, 3-MA or rapamycin.

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The present study aimed to prepare a kind of controlled-releasing insulin-like growth factor 1 (IGF-1)/spider silk protein nanofibrous membrane using a electrostatic spinning method and evaluated its effect on the cell viability of endothelial progenitor cells (EPCs). Recombinant spidroin named as GMCDRSSP-IgF-1 was electro-spun into nanofibrous membrane which can be degraded by protease and be capable of sustained-release of IGF-1. The membrane can be degraded after being treated with thrombin.

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This study examined the effects of Stmn2 on phenotype transformation of vascular smooth muscle in vascular injury via RNA sequencing and experimental validation. Total RNA was extracted for RNA sequencing after 1, 3 and 5 days of injury to screen the differentially expressed genes (DEGs). Western blot was used to detect the protein expression of Stmn2 and its associated targets.

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Accumulating evidence has shown that endothelial progenitor cell-derived exosomes (EPC-Exos) can ameliorate myocardial fibrosis. The purpose of the present study was to investigate the effects of EPC-Exos-derived microRNAs (miRNAs) on myocardial infarction (MI). A miRNA-Seq dataset of miRNAs differentially expressed between EPCs and exosomes was collected.

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Background: Ischemia/reperfusion-mediated myocardial infarction (MIRI) is a major pathological factor implicated in the progression of ischemic heart disease, but the key factors dysregulated during MIRI have not been fully elucidated, especially those essential non-coding factors required for cardiovascular development.

Methods: A murine MIRI model and RNA sequencing (RNA-seq) were used to identify key lncRNAs after myocardial infarction. qRT-PCR was used to validate expression in cardiac muscle tissues and myocardial cells.

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Myocardial infarction (MI) remains a leading cause of morbidity and mortality worldwide. Endothelial progenitor cell (EPC)-derived exosomes have been found to be effective in alleviating MI, while the detailed mechanisms remain unclear. The present study aimed to determine the protective effects of EPC-derived exosomal miR-1246 and miR-1290 on MI-induced injury and to explore the underlying molecular mechanisms.

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Aim: Diabetic nephropathy (DN) is a serious health problem worldwide. Epidermal growth factor (EGF) has suggested as a potential biomarker for the progression of chronic kidney disease. In this study, we examined the effects of EGF on the high glucose (HG)-induced podocyte injury and explored the underlying molecular mechanisms.

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The Long Noncoding RNA RP11-728F11.4 Promotes Atherosclerosis.

Arterioscler Thromb Vasc Biol

March 2021

Department of Clinical Laboratory, Guangzhou Women and Children Medical Center, Guangzhou Medical University, China (X.-H.D., Y.-W.H.).

Objective: Noncoding RNAs are emerging as important players in gene regulation and cardiovascular diseases. Their roles in the pathogenesis of atherosclerosis are not fully understood. The purpose of this study was to determine the role played by a previously uncharacterized long noncoding RNA, RP11-728F11.

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Importance of βAR elevation for re-endothelialization capacity mediated by late endothelial progenitor cells in hypertensive patients.

Am J Physiol Heart Circ Physiol

February 2021

Department of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen, (Shenzhen Sun Yat-sen Cardiovascular Hospital), Shenzhen, China.

Dysfunction of late endothelial progenitor cells (EPCs) has been suggested to be associated with hypertension. β-Adrenergic receptor (βAR) is a novel and key target for EPC homing. Here, we proposed that attenuated βAR signaling contributes to EPCs dysfunction, whereas enhanced βAR signaling restores EPCs' functions in hypertension.

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