Cardiovascular Therapeutics最新文献

{"title":"Verteporfin Mitigates Isoproterenol-Induced Myocardial Hypertrophy by Attenuating IL-6/STAT3 in Cardiac Fibroblasts","authors":"Sunpeng Sheng,&nbsp;Lu Ding,&nbsp;Jinbiao Lai,&nbsp;Zelei Ye,&nbsp;Ru Zhao,&nbsp;Shijia Chen,&nbsp;Jianshe Ma,&nbsp;Junming Fan,&nbsp;Peifeng Jin","doi":"10.1155/cdr/2852780","DOIUrl":"https://doi.org/10.1155/cdr/2852780","url":null,"abstract":"<p><b>Background:</b> Yes-associated protein (YAP) is a major downstream nuclear coactivator of the Hippo pathway and is activated during myocardial hypertrophy. Verteporfin, a YAP inhibitor, may serve as a potential treatment for myocardial hypertrophy.</p><p><b>Aim:</b> This study was aimed at exploring the role and underlying mechanisms of verteporfin in isoproterenol (ISO)-induced myocardial hypertrophy both in vivo and in vitro.</p><p><b>Methods:</b> GSE18801 directs our focus toward the Hippo pathway role in myocardial hypertrophy. Using an ISO-induced myocardial hypertrophy rat model, YAP expression and localization were observed through Western blot and immunofluorescence. Histopathological analysis was performed to evaluate cardiomyocyte cross-sectional area, and echocardiographic examinations were conducted to assess cardiac function. In vitro, primary neonatal rat cardiomyocytes (NRCMs) were cultured with conditioned medium from cardiac fibroblasts (CF-CM) treated with ISO to observe cell hypertrophy. Mechanistically, GSE203358 dataset analysis, enzyme-linked immunosorbent assay (ELISA), and Western blot were utilized to investigate the effects of ISO and verteporfin on IL-6, STAT3, and p-STAT3 levels in CFs. Subsequently, the changes in the IL-6/STAT3 pathway were evaluated in CFs treated with ISO and verteporfin. Additionally, recombinant IL-6 and IL-6 inhibitor were applied to CMs treated with CF-CM to observe changes in cardiomyocyte size.</p><p><b>Results:</b> Verteporfin improved cardiac performance in rats receiving ISO. In cultured NRCM, both ISO and CF-CM treated with ISO could induce cardiomyocyte hypertrophy. Verteporfin did not attenuate ISO-induced cardiomyocyte hypertrophy. However, it could attenuate hypertrophy induced by the CF-CM treated with ISO. GSE203358 indicated the involvement of the IL-6/STAT3 pathway in the presence of verteporfin in CFs. Additionally, verteporfin reduces IL-6 production in cultured CFs subjected to ISO treatment. Notably, the effects of verteporfin on NRCM were reversed by IL-6.</p><p><b>Conclusions:</b> Verteporfin protects the heart against ISO-induced myocardial hypertrophy by regulating IL-6/STAT3 in cardiac fibroblasts.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/2852780","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144910499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Application Value of Brain Natriuretic Peptide in the Prognostic Evaluation of Patients With Chronic Left Heart Failure","authors":"Congling Xiang,&nbsp;Weier Zhou","doi":"10.1155/cdr/9353377","DOIUrl":"https://doi.org/10.1155/cdr/9353377","url":null,"abstract":"<p>This study explores the predictive utility of brain natriuretic peptide (BNP) levels in assessing outcomes for patients with chronic left heart failure (LHF). A cohort of 59 patients diagnosed with chronic LHF was compared to 59 healthy controls. BNP levels, alongside other cardiac function parameters, such as left ventricular ejection fraction (LVEF) and left ventricular end-systolic dimension (LVESD), were evaluated. Results revealed that BNP levels were positively correlated with worsening cardiac function and negatively correlated with LVEF. In individuals with obesity or Type 2 diabetes mellitus, BNP levels were unexpectedly lower, whereas patients with chronic kidney disease or atrial fibrillation exhibited elevated BNP levels. A BNP cut-off value of 98.9 was identified, demonstrating high diagnostic sensitivity (91.53%), specificity (83.05%), and accuracy (88.14%). The area under the ROC curve (AUC) indicated strong diagnostic performance for BNP in predicting adverse cardiovascular events. The findings underscore BNP’s value not only as a biomarker for diagnosing LHF but also in prognostication and tailoring patient-specific interventions. Future studies should validate these findings across diverse populations to enhance clinical application.</p><p><b>Trial Registration:</b> Chinese Clinical Trial Registry identifier: ChiCTR2500101966</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/9353377","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144853798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heart Rate Variability’s Value in Predicting Out-of-Hospital Major Adverse Cardiovascular Events in Patients With Chronic Heart Failure","authors":"Li Men,&nbsp;Bingxin Chen,&nbsp;Long Yang,&nbsp;Jiangrong Shi,&nbsp;Shuqin Tang,&nbsp;Xing Jiang,&nbsp;Yunhua Chen,&nbsp;Xiao Wang,&nbsp;Ping Fan","doi":"10.1155/cdr/6412775","DOIUrl":"https://doi.org/10.1155/cdr/6412775","url":null,"abstract":"<p><b>Background:</b> Chronic heart failure (CHF) involves changes in cardiac structure and function, along with extensive neuroendocrine adaptations and metabolic abnormalities. Heart rate variability (HRV) is a noninvasive measure of autonomic nervous system function and is associated with mortality in CHF. However, the significance of HRV in predicting major adverse cardiovascular events (MACEs) in CHF patients has not been fully explored. This study was aimed at investigating the predictive value of HRV parameters assessed by 24-h Holter monitoring for MACEs in CHF patients.</p><p><b>Methods:</b> This prospective cohort study included 906 CHF patients from five centers in Xinjiang, China, who underwent Holter monitoring and were followed up. Cox proportional hazards regression models were used to assess the independent associations between HRV parameters and the incidence of MACEs. Receiver operating characteristic (ROC) curve analysis was conducted to determine the predictive accuracy of each HRV parameter, and the incremental predictive value of HRV parameters was evaluated using coherence index (<i>C</i>-index), net reclassification improvement (NRI), and integrated discrimination improvement (IDI).</p><p><b>Results:</b> During a median follow-up of 16 months, 211 (23.3%) MACEs occurred. Cox regression analysis indicated that SDNN (HR: 0.976, 95% CI: 0.970~0.981), triangular index (HR: 0.963, 95% CI: 0.953~0.973), SDNN index (HR: 0.983, 95% CI: 0.974~0.992), SDANN index (HR: 0.974, 95% CI: 0.967~0.981), NN50 (HR: 0.859, 95% CI: 0.787~0.937), rMSSD (HR: 0.980, 95% CI: 0.970~0.989), TP (HR: 0.890, 95% CI: 0.816~0.971), VLF (HR: 0.889, 95% CI: 0.815~0.969), LF (HR: 0.817, 95% CI: 0.743~0.898), and HF (HR: 0.806, 95% CI: 0.728~0.893) were independently associated with MACEs. ROC analysis revealed that the triangular index and SDNN had the highest area under the curve (AUC) for predicting MACEs, with values of 0.699 (95% CI: 0.655~0.743) and 0.711 (95% CI: 0.668~0.753), respectively. Incorporation of HRV parameters into traditional risk models improves the <i>C</i>-index, NRI, and IDI of the model’s predictive ability for MACE and cardiovascular mortality to varying degrees.</p><p><b>Conclusion:</b> SDNN and triangular index demonstrated the strongest predictive abilities; other time–domain and frequency–domain parameters also showed certain predictive values for MACEs.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/6412775","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144832629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correlation and Influencing Factor Analysis Between Gal-3 and Recurrent Patients With Nonvalvular Atrial Fibrillation After Radiofrequency Ablation","authors":"Jing Lu,&nbsp;Fan Yang,&nbsp;Yu Gao,&nbsp;Ruijuan Li,&nbsp;Runqin Li,&nbsp;Nan Zhang,&nbsp;Yan Ren,&nbsp;Dengfeng Ma","doi":"10.1155/cdr/5561883","DOIUrl":"https://doi.org/10.1155/cdr/5561883","url":null,"abstract":"<p><b>Aims:</b> This prospective cohort study was aimed at evaluating the association of galectin-3 (Gal-3) and other prognostic factors with atrial fibrillation (AF) recurrence in patients with nonvalvular AF undergoing radiofrequency catheter ablation (RFCA).</p><p><b>Methods and Results:</b> Overall, 92 patients were included, with the AF group comprising 70 patients and the control group comprising 20 (supraventricular tachycardic) patients. Preablation parameters were recorded, including baseline Gal-3 levels. Patients were followed up for 6 months post-RFCA. AF recurrence was defined as AF episodes lasting &gt; 30 s after the blanking period. Univariate and multivariate logistic regression analyses revealed patients with AF were older and significantly hypertensive (<i>p</i> &lt; 0.05) when compared to control. Gal-3 levels were significantly higher in the paAF (13.81 ± 2.56) and peAF (15.92 ± 3.67) groups than in the control group (12.04 ± 3.28). Recurrence occurred in 28 patients (40%) with AF. Baseline Gal-3 levels were higher in the recurrence group than in the nonrecurrence group. Univariate analysis revealed left atrial diameter (LAD), left atrial volume (LAV), high-sensitivity C-reactive protein (hs-CRP), Gal-3, and LV short-axis shortening rate as significant predictors of AF recurrence. However, multivariate analyses showed only LAV (OR = 1.043 [1.011–1.077]; <i>p</i> = 0.009), hs-CRP (OR = 1.176 [1.025–1.349], <i>p</i> = 0.021), and Gal-3 (OR = 2.019 [1.332–3.06], <i>p</i> = 0.001) as independent predictors of recurrence.</p><p><b>Conclusion:</b> Elevated Gal-3 and hs-CRP levels along with increased LAV are predictive of AF recurrence, irrespective of AF type. This finding holds a significant potential for guiding therapeutic strategies in clinical practice.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/5561883","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144833198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Significance of APOB/APOA1 Ratio in the Prediction of Calcific Aortic Valve Disease","authors":"Yuxing Wang,&nbsp;Ming Yu,&nbsp;Song Yang,&nbsp;Jiajie Mei,&nbsp;Zhenzhu Liu,&nbsp;Zhaohong Geng,&nbsp;Wenli Xie,&nbsp;Lijiao Zhang,&nbsp;Hongyan Wang,&nbsp;Nan Niu,&nbsp;Peng Qu","doi":"10.1155/cdr/5528174","DOIUrl":"https://doi.org/10.1155/cdr/5528174","url":null,"abstract":"<p><b>Background:</b> Calcific aortic valve disease (CAVD) is a prevalent heart valve disease. The ratio of two apolipoproteins with distinct functions, Apolipoprotein B/Apolipoprotein A1 (APOB/APOA1), has been proposed as a novel assessment index for the evaluation of cardiovascular diseases. The aim of this article is to discuss the role of lipid parameters such as APOB/APOA1 in CAVD and the risk factors for CAVD, to develop a predictive model for CAVD, and to evaluate the sensitivity and specificity of this model.</p><p><b>Method:</b> Patients who initially presented to the Department of Cardiology of the Second Affiliated Hospital of Dalian Medical University between 1 January 2023 and 31 December 2023 were retrospectively identified and included in the study. Patients were divided into an aortic valve calcification group (111 cases) and a control group (201 cases) based on computed tomography (CT) findings. The clinical data, laboratory examination results, and chest CT images of the patients were collected and analyzed. A variety of statistical methods were used to analyze risk factors for CAVD, to construct a CAVD prediction model, and to assess its sensitivity and specificity.</p><p><b>Results:</b> Lipid parameters APOA1, APOB/APOA1, cumulative low-density lipoprotein (LDL) exposure, and non–high-density lipoprotein/high-density lipoprotein (non-HDL/HDL) were significantly associated with aortic valve calcification. Age, history of diabetes, diastolic blood pressure (DBP), APOB/APOA1, Cystatin C (Cys-c), and neutrophil-to-lymphocyte ratio (NLR) are identified as independent risk factors for CAVD, and the combined model achieved an AUC of 0.796 for CAVD prediction, corresponding to a sensitivity of 0.769 and a specificity of 0.755.</p><p><b>Conclusion:</b> The lipid parameters APOA1, APOB/APOA1, cumulative LDL exposure, and non-HDL/HDL have been demonstrated to be associated with aortic valve calcification. Furthermore, APOB/APOA1 can be used for the prediction of CAVD, and the combination of APOB/APOA1 with age, history of diabetes, DBP, Cys-c, and NLR has better prediction performance for CAVD.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/5528174","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144767811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Wogonin Inhibits Cardiac Hypertrophy by Activating Nrf-2-Mediated Antioxidant Responses”","authors":"","doi":"10.1155/cdr/9864046","DOIUrl":"https://doi.org/10.1155/cdr/9864046","url":null,"abstract":"<p>X. Shi, B. Zhang, Z. Chu, et al., “Wogonin Inhibits Cardiac Hypertrophy by Activating Nrf-2-Mediated Antioxidant Responses”, <i>Cardiovascular Therapeutics</i> 2021 (2021): 9995342, https://doi.org/10.1155/2021/9995342</p><p>In the article, there is an error in Figure 4e due to the incorrect selection of images during manuscript preparation. The correct Figure 4 is shown below:</p><p>The authors apologize for this error.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/9864046","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144740507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eplerenone Inhibits Atrial Autonomic Nerve Remodeling in Atrial Fibrillation Through ERK1/2 MAPK Pathway","authors":"Wei Xu,&nbsp;Cheng-yuan Yu,&nbsp;Ding-yu Wang,&nbsp;Qiang Gao,&nbsp;Song Zhang,&nbsp;Yun Zhang,&nbsp;Yue Yuan,&nbsp;Jing Shi,&nbsp;Yue Li,&nbsp;Guang-zhong Liu,&nbsp;Xiao-ming Shang","doi":"10.1155/cdr/6041636","DOIUrl":"https://doi.org/10.1155/cdr/6041636","url":null,"abstract":"<p>Atrial autonomic nerve system (ANS) remodeling plays an important role in atrial fibrillation (AF). Mineralocorticoid receptor antagonists (MRAs) have been proved to be effective in preventing atrial structural remodeling. However, the effects of MRA on ANS remodeling in AF and the underlying mechanisms are still unknown.</p><p><b>Methods:</b> Then, 21 rabbits were randomized into sham, pacing, and pacing + eplerenone groups. To verify the effect of aldosterone on ANS remodeling, 18 SD rats were pumped with aldosterone. HL-1 cells were subjected to control treatment or rapid pacing with or without eplerenone or U0126 (an inhibitor of ERK1/2). Atrial sympathetic and parasympathetic remodeling was detected by immunohistochemical staining, Western blotting, and RT-PCR. The circulating neurohormone and atrial electrophysiology were also assessed.</p><p><b>Results:</b> The ERK1/2 MAPK pathway was significantly activated in AF rabbit/HL-1 cell models, resulting in the upregulation of key downstream protein; this effect was significantly restored by eplerenone. Eplerenone prevented the alterations in circulating neurohormone, reduced the mRNA level of sympathetic and parasympathetic-related growth factors, and inhibited the inducibility and duration of AF.</p><p><b>Conclusions:</b> Eplerenone inhibited atrial autonomic nerve remodeling and the occurrence of AF through modulating the ERK1/2 MAPK pathway.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/6041636","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144714843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rivaroxaban Ameliorates Sunitinib-Induced Injury of Cardiomyocytes via Repressing MAPK Signaling Pathway","authors":"Ying Qian,&nbsp;Fang Yi","doi":"10.1155/cdr/2208110","DOIUrl":"https://doi.org/10.1155/cdr/2208110","url":null,"abstract":"<p><b>Background:</b> Sunitinib (SU) is used to treat kidney cancer. However, it can also cause cardiotoxicity. This study is performed to investigate whether rivaroxaban (RIV) attenuates SU-induced cardiotoxicity (SIC).</p><p><b>Methods and Materials:</b> AC16 cells and primary cardiomyocytes of neonatal mouse were treated with different concentrations (2–10 <i>μ</i>M) of SU for 24 h or with 6 <i>μ</i>M SU and 10 <i>μ</i>g/mL RIV for 24 h. The viability of cardiomyocytes was evaluated using the cell counting kit-8 (CCK-8) assay, and the apoptosis rate was evaluated using flow cytometry. The activity of caspase-3 was determined. The levels of malondialdehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD) were also measured. The potential targets and downstream pathways of RIV in SIC treatment were investigated using network pharmacology, molecular docking, and molecular dynamics simulation. qPCR and western blotting were used to detect the regulatory effects of SU and RIV on mRNA and protein expression of MAPK pathway-related genes, respectively.</p><p><b>Results:</b> RIV treatment alleviated SU-induced cardiomyocyte injury by promoting viability and inhibiting apoptosis, oxidative stress, and the inflammatory response in AC16 cells and primary cardiomyocytes. Caspase 3 (CASP3), signal transducer and activator of transcription 3 (STAT3), SRC proto-oncogene, nonreceptor tyrosine kinase (SRC), ATP-binding cassette subfamily G member 2 (ABCG2), and ATP-binding cassette subfamily B member 1 (ABCB1) were candidate targets of RIV in SIC. The binding affinities between RIV and CASP3, STAT3, SRC, ABCG2, and ABCB1 were all less than −7.5 kcal/mol, indicating that RIV could bind stably to these targets. Bioinformatics analyses suggested that the mitogen-activated protein kinase (MAPK) pathway was involved in the mechanism by which RIV alleviated SIC. RIV treatment decreased the mRNA expression of CASP3 and increased the mRNA expression of STAT3, SRC, ABCG2, and ABCB1 in AC16 cells and primary cardiomyocytes. RIV also inhibited the SU-induced activation of the MAPK pathway.</p><p><b>Conclusion:</b> RIV exerts a protective effect against SU-induced cardiomyocyte injury by inhibiting the MAPK signaling pathway. RIV therapy may be a promising strategy to inhibit SU’s cardiotoxicity in cancer patients.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/2208110","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144705354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kynurenic Acid Is a Predictive Prognostic Metabolic Marker in ST-Elevation Myocardial Infarction","authors":"Xiaolin Zhang,&nbsp;Miaohan Qiu,&nbsp;Kun Na,&nbsp;Minghui Cheng,&nbsp;Haixu Song,&nbsp;Ning Zhao,&nbsp;Dan Liu,&nbsp;Chenghui Yan,&nbsp;Yaling Han","doi":"10.1155/cdr/9123654","DOIUrl":"https://doi.org/10.1155/cdr/9123654","url":null,"abstract":"<p><b>Background:</b> The tryptophan/kynurenic acid (KYNA) pathway plays a crucial role by modulating inflammation, oxidative stress, and immune activation. The clinical value of tryptophan metabolites in the KYNA pathway for the early diagnosis and prognosis of STEMI patients, as well as the underlying functional mechanisms, remains to be elucidated.</p><p><b>Objectives:</b> This study evaluated the prognostic value of KYNA, a metabolite of the tryptophan pathway, in STEMI patients.</p><p><b>Methods:</b> Untargeted metabolomics by ¹H-nuclear magnetic resonance (NMR) analysis was used to examine metabolite changes between 50 control subjects and 50 STEMI patients with an onset time of &lt; 3 h. Furthermore, targeted metabolomic analysis was employed to investigate the association between KYNA and the prognosis of STEMI patients by LC-Q-TOF MS analysis.</p><p><b>Results:</b> Fifteen differential metabolites were identified between STEMI patients and control subjects by ¹H-NMR analysis. KYNA as an important metabolite upregulated obviously in the tryptophan pathway was 337.67 nmol/L in STEMI patients (interquartile range: 241.16–500.29 nmol/L). In addition, KYNA was significantly associated with major adverse cardiovascular events (MACEs) (HR: 5.95, 95% CI: 2.03–17.44; <i>p</i> = 0.0012) and all-cause mortality (HR: 7.11, 95% CI: 1.52–33.29; <i>p</i> = 0.013) and showed moderate predictive value for 12-month MACE (area under the curve (AUC) = 0.72, 95% CI: 0.65–0.80) and all-cause mortality (AUC = 0.74, 95% CI: 0.65–0.83). KAT1 expression was upregulated in infiltrating macrophages of thrombus tissue coming from the culprit coronary artery of STEMI patients. KAT1 upregulation was also observed in macrophages located within the peri-infarct myocardium.</p><p><b>Conclusions:</b> The KYNA level may correspond to the underlying status of acute myocardial infarction and is a promising biomarker for predicting STEMI progression.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/9123654","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144647602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astragaloside IV Alleviates H2O2-Induced Mitochondrial Dysfunction and Inhibits Mitophagy Via PI3K/AKT/mTOR Pathway","authors":"Miaomiao Qi,&nbsp;Qiongying Wang,&nbsp;Runmin Sun,&nbsp;Zeyi Cheng,&nbsp;Mingze Li,&nbsp;Xin Fan,&nbsp;Feng Bai,&nbsp;Jing Yu","doi":"10.1155/cdr/9549175","DOIUrl":"https://doi.org/10.1155/cdr/9549175","url":null,"abstract":"<p>Oxidative stress and mitochondrial dysfunction play critical roles in the pathology of cardiovascular diseases. However, the effects of Astragaloside IV (As-IV) on mitochondrial function remain unclear. This study is aimed at evaluating the protective effects and mechanism of As-IV against H₂O₂-induced mitochondrial dysfunction in H9c2 cells. H9c2 cells were exposed to 200 <i>μ</i>M H₂O₂ with or without As-IV. The level of apoptosis and reactive oxygen species (ROS) was measured by flow cytometry. Confocal microscopy and transmission electron microscopy were performed to detect the changes in mitochondrial membrane potential (MMP), mitochondrial morphology, and autophagosome. Mitochondrial dynamics and mitophagy-related proteins were measured by Western blot. The results indicated that As-IV decreased H₂O₂-induced apoptosis and ROS generation. Meanwhile, As-IV significantly increased MMP, exerted regulatory effects on mitochondrial dynamics, and ameliorated the damaged mitochondrial morphology in H₂O₂-injured cardiomyocytes. Additionally, As-IV decreased the amount of autophagosome and expressions of PINK1 and Parkin, but upregulated the expressions of PI3K, p-AKT, and p-mTOR proteins. However, cotreatment with LY294002 diminished the upregulation of PI3K, p-AKT, and p-mTOR induced by As-IV. In the study, we demonstrated that As-IV protected H9c2 cells from H₂O₂-induced mitochondrial dysfunction by inhibiting mitophagy, which might be related to the PI3K/AKT/mTOR pathway.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2025 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cdr/9549175","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144589902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}