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Yuan Jiang

Bio: Yuan Jiang is an academic researcher from Sun Yat-sen University. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 1, co-authored 8 publications receiving 1 citations.

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Journal ArticleDOI
27 Jun 2022-ACS Nano
TL;DR: Copper sulfide/titanium oxide heterostructure nanosheets modified with hyaluronic acid and PEG provide a macrophage-targeting sonodynamic/photothermal synergistic therapy, which is an effective translational clinical intervention for early atherosclerotic plaques.
Abstract: Sonodynamic therapy (SDT) and photothermal therapy (PTT) are two effective strategies for the treatment of atherosclerotic plaques. However, the low yield of reactive oxygen species (ROS) of conventional organic sonosensitizers and the low biosafety of hyperthermia limit the therapeutic efficacy of SDT and PTT. Herein, we report copper sulfide/titanium oxide heterostructure nanosheets modified with hyaluronic acid (HA) and PEG (HA-HNSs) for low-intensity sonodynamic and mild-photothermal synergistic therapy for early atherosclerotic plaques. CuS/TiO2 heterostructure nanosheets (HNSs) show high electron-hole separation efficiency and superior sonodynamic performance, because it has high surface energy crystal facets as well as a narrow band. Moreover, HNSs exhibit intense absorbance in the NIR-II region, which endows the nanosheets with excellent photothermal performance. With a further modification of HA, HA-HNSs can selectively target intraplaque proinflammatory macrophages through CD44-HA interaction. Because SDT reduces the expression of heat shock protein 90 and PTT facilitates the sonocatalytic process, the combination of SDT and PTT based on HA-HNSs could synergistically induce proinflammatory macrophage apoptosis. More importantly, the synergistic therapy prevents the progression of early atherosclerotic plaque by removing lesional macrophages and mitigating inflammation. Taken together, this work provides a macrophage-targeting sonodynamic/photothermal synergistic therapy, which is an effective translational clinical intervention for early atherosclerotic plaques.

22 citations

Journal ArticleDOI
TL;DR: Wang et al. as discussed by the authors explored the role of glycolysis in cardiac fibroblast activation and cardiac fibrosis after myocardial infarction (MI), and showed that 2-Deoxy-D-glucose (2-DG) could significantly inhibit the increased expression of both the gly colytic and fibrotic proteins in the activated CF.
Abstract: Objective: To explore the role of glycolysis in cardiac fibroblast (CF) activation and cardiac fibrosis after myocardial infarction (MI). Method: In vivo: 2-Deoxy-D-glucose (2-DG), a glycolysis inhibitor, was injected into the abdominal cavity of the MI or sham mice every day. On the 28th day, cardiac function was measured by ultrasonic cardiography, and the hearts were harvested. Masson staining and immunofluorescence (IF) were used to evaluate the fibrosis area, and western blot was used to identify the glycolytic level. In vitro, we isolated the CF from the sham, MI and MI with 2-DG treatment mice, and we also activated normal CF with transforming growth factor-β1 (TGF-β1) and block glycolysis with 2-DG. We then detected the glycolytic proteins, fibrotic proteins, and the concentrations of lactate and glucose in the culture medium. At last, we further detected the fibrotic and glycolytic markers in human fibrotic and non-fibrotic heart tissues with masson staining, IF and western blot. Result: More collagen and glycolytic protein expressions were observed in the MI mice hearts. The mortality increased when mice were treated with 2-DG (100 mg/kg/d) after the MI surgery (Log-rank test, P < 0.05). When the dosage of 2-DG declined to 50 mg/kg/d, and the treatment was started on the 4th day after MI, no statistical difference of mortality between the two groups was observed (Log-rank test, P = 0.98). The collagen volume fraction was smaller and the fluorescence signal of α-smooth muscle actin (α-SMA) was weaker in mice treated with 2-DG than PBS. In vitro, 2-DG could significantly inhibit the increased expression of both the glycolytic and fibrotic proteins in the activated CF. Conclusion: Cardiac fibrosis is along with the enhancement of CF activation and glycolysis. Glycolysis inhibition can alleviate cardiac fibroblast activation and cardiac fibrosis after myocardial infarction.

16 citations

Journal ArticleDOI
TL;DR: Ventricular arrhythmia and SCD resulted as a common occurrence with a high prevalence in patients with COVID-19 admitted to the hospital and significantly contributed to an increased risk of death in hospitals with CO VID-19.
Abstract: Background Arrhythmia is a very common complication of coronavirus disease 2019 (COVID-19); however, the prevalence of ventricular arrhythmia and associated outcomes are not well-explored. Here, we conducted a systematic review and meta-analysis to determine the prevalence and associated death of ventricular arrhythmia and sudden cardiac death (SCD) in patients with COVID-19. Methods Databases of PubMed, Cochrane Library, Embase, and MdeRxiv were searched. Studies that could calculate the prevalence of ventricular arrhythmia/SCD during hospital admission or associated death in patients with COVID-19 were included. The study was registered with the PROSPERO (CRD42021271328). Results A total of 21 studies with 13,790 patients were included. The pooled prevalence of ventricular arrhythmia was 5% (95% CI: 4–6%), with a relatively high-SCD prevalence (1.8% in hospitalized COVID-19 and 10% in deceased cases of COVID-19). Subgroup analysis showed that ventricular arrhythmia was more common in patients with elevated cardiac troponin T [ES (effect size): 10%, 95% CI: −0.2 to 22%] and in European (ES: 20%, 95% CI: 11–29%) populations. Besides, ventricular arrhythmia was independently associated with an increased risk of death in patients with COVID-19 [odds ratio (OR) = 2.83; 95% CI: 1.78–4.51]. Conclusion Ventricular arrhythmia and SCD resulted as a common occurrence with a high prevalence in patients with COVID-19 admitted to the hospital. Furthermore, ventricular arrhythmia significantly contributed to an increased risk of death in hospitalized patients with COVID-19. Clinicians might be vigilant of ventricular arrhythmias for patients with COVID-19, especially for severe cases. Systematic Review Registration www.york.ac.uk/inst/crd, identifier: CRD42021271328.

8 citations

Journal ArticleDOI
TL;DR: NSAIDs might provide a survival benefit, although they might potentially increase the risk of stroke, when used prior to admission or diagnosis of COVID‐19, based on current evidence.
Abstract: Recent reports of potential harmful effects of nonsteroidal anti‐inflammatory drugs (NSAIDs) in treating patients with coronavirus disease 2019 (COVID‐19) have raised great concern.

7 citations

Journal ArticleDOI
TL;DR: Among patients with HFpEF, the risk of advanced liver fibrosis is associated with an increased incidence of new-onset atrial fibrillation (AF) and may be a novel predictor for new-ONSet AF.
Abstract: Non‐alcoholic fatty liver disease (NAFLD)‐related advanced liver fibrosis (Stage 3 or 4) was reported to be linked to worse prognosis in patients with heart failure with preserved ejection fraction (HFpEF). This study aims to assess the relationship between liver fibrosis scores and new‐onset atrial fibrillation (AF) incidence in patients with HFpEF in the Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist (TOPCAT) trial.

6 citations


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TL;DR: The recent advancements that emphasize the critical role of SIRT3 as a master regulator of cardiac metabolism are summarized and a comprehensive view of all known activators of Sirtuin 3 is presented, to elaborate on their therapeutic potential to ameliorate energetic abnormalities in various cardiac pathologies.
Abstract: The heart is a highly metabolically active organ that predominantly utilizes fatty acids as an energy substrate. The heart also derives some part of its energy by oxidation of other substrates, including glucose, lactose, amino acids and ketones. The critical feature of cardiac pathology is metabolic remodeling and loss of metabolic flexibility. Sirtuin 3 (SIRT3) is one of the seven mammalian sirtuins (SIRT1 to SIRT7), with NAD+ dependent deacetylase activity. SIRT3 is expressed in high levels in healthy hearts but downregulated in the aged or diseased hearts. Experimental evidence shows that increasing SIRT3 levels or activity can ameliorate several cardiac pathologies. The primary deacetylation targets of SIRT3 are mitochondrial proteins, most of which are involved in energy metabolism. Thus, SIRT3 improves cardiac health by modulating cardiac energetics. In this review, we discuss the essential role of SIRT3 in regulating cardiac metabolism in the context of physiology and pathology. Specifically, we summarize the recent advancements that emphasize the critical role of SIRT3 as a master regulator of cardiac metabolism. We also present a comprehensive view of all known activators of SIRT3, and elaborate on their therapeutic potential to ameliorate energetic abnormalities in various cardiac pathologies.

10 citations

Journal ArticleDOI
TL;DR: In this paper , a PEGylated CuxMnySz (PCMS) nanocatalyst was proposed to promote cascade catalytic reactions in tumor microenvironment (TME) while confining offtarget side effects on normal tissues.
Abstract: Nanocatalysts, a class of nanomaterials with intrinsic enzyme‐like activities, have been widely investigated for cancer catalytic therapy in recent years. However, precise construction of nanocatalysts with excellent enzyme catalytic activity and biosafety for tumor therapy still remains challenging. Here, a biodegradable nanocatalyst, PEGylated CuxMnySz (PCMS), is reported that can promote cascade catalytic reactions in tumor microenvironment (TME) while confining off‐target side effects on normal tissues. PCMS not only catalyzes the cascade conversion of endogenous hydrogen peroxide (H2O2) to oxygen (O2) via catalase‐like activity and then to superoxide radical (·O2−) via oxidase‐like activity in the TME, but also effectively depletes intracellular glutathione via glutathione oxidase‐like activity. The cascade catalytic reactions, by taking advantage of high H2O2 level in tumor cells, result in an enhanced enzyme catalytic effect in generation of ·O2−. More importantly, PCMS exhibits prominent photothermal effect under NIR‐II 1064 nm laser irradiation that can further enhance chemodynamic therapy (CDT) efficacy in tumors. In addition, the biodegradation in TME and excellent photothermal effect of PCMS are beneficial to magnetic resonance imaging, photoacoustic imaging and infrared thermal imaging, resulting in tracing the fate of PCMS in vivo. This study provides a new tool for rational design of TME‐responsive nanocatalysts with high biocompatibility for tumor catalytic therapy.

8 citations

Journal ArticleDOI
TL;DR: Among patients with HFpEF, the risk of advanced liver fibrosis is associated with an increased incidence of new-onset atrial fibrillation (AF) and may be a novel predictor for new-ONSet AF.
Abstract: Non‐alcoholic fatty liver disease (NAFLD)‐related advanced liver fibrosis (Stage 3 or 4) was reported to be linked to worse prognosis in patients with heart failure with preserved ejection fraction (HFpEF). This study aims to assess the relationship between liver fibrosis scores and new‐onset atrial fibrillation (AF) incidence in patients with HFpEF in the Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist (TOPCAT) trial.

6 citations

Journal ArticleDOI
TL;DR: In patients with nonalcoholic fatty liver disease, liver fibrosis was associated with a higher risk of cardiovascular events and the relationship between liver Fibrosis scores and clinical outcomes in patients with cardiovascular disease remains unclear.
Abstract: In patients with nonalcoholic fatty liver disease, liver fibrosis was associated with a higher risk of cardiovascular events. However, the relationship between liver fibrosis scores and clinical outcomes in patients with cardiovascular disease remains unclear.

5 citations