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Coronary artery disease (CAD), a widespread cardiovascular ailment, exhibits a strong association with palmitoylation. This research aimed to elucidate the role of S-palmitoylation in CAD through bioinformatics, providing novel perspectives on the mechanism underlying CAD. By intersecting differentially expressed genes with weighted gene co-expression network analysis (WGCNA) from the GSE113079 dataset, 534 differentially expressed palmitoylation-related genes (DE-PRGs) were identified. Protein-protein interaction (PPI) network analysis, in conjunction with machine learning algorithms and immune infiltration analysis utilizing CIBERSORT, identified CXCL12, KRTAP4-7, and PPP2R2B as pivotal hub genes in CAD progression with significant immune links. Enrichment analyses revealed their predominant roles in immune regulation. Nomogram and ROC curve analyses revealed robust diagnostic predictive capabilities grounded in the three hub genes. A regulatory network involving the transcription factor HDAC2 and miRNA hsa-mir-23a-3p was predicted. Single-cell sequencing (GSE121893) further highlighted endothelial cells, fibroblasts, and macrophages as central cellular interactors, with significant crosstalk among these populations. These findings positioned CXCL12, KRTAP4-7 and PPP2R2B as key palmitoylated hub genes in CAD, thereby offering dual potential as diagnostic markers and therapeutic targets.

Inflammation is a common characteristic of chronic liver disease (CLD). Inflammasomes are multiprotein complexes that can sense and recognize various exogenous and endogenous danger signals, eventually activating interleukin (IL)-1β and IL-18. The sensor component of the inflammasome system is a nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs). The NLRs family pyrin domain containing 3 (NLRP3) inflammasome has been involved in the initiation and progression of CLD. However, the molecular mechanisms by which it triggers liver inflammation and damage remain unclear. Here, we focus on recent advances on the potential role of NLRP3 inflammasome activation in the progression of CLD, including viral hepatitis, non-alcoholic steatohepatitis and alcoholic liver disease, and in particular, its ability to alleviate liver inflammation in animal models. Additionally, we also discuss various pharmacological inhibitors identifying the NLRP3 inflammasome signaling cascade as novel therapeutic targets in the treatment of CLD. In summary, this review summarizes the relevance of the NLRP3 inflammasome in the initiation and progression of CLD, and provides critical targets to suppress the development of CLD in clinical management.

C1q/tumor necrosis factor-related protein 9 (CTRP9) has been recognized as a factor associated with cardiovascular disease. Nevertheless, research regarding its relationship with the severity of coronary artery disease and the occurrence of adverse clinical events in coronary atherosclerotic heart disease (CAD) remains limited. A total of 302 patients were divided into mild lesion group and moderate-severe lesion group according to coronary artery complexity, determined by the SYNTAX scores. Major adverse cardiovascular events (MACEs) were assessed during a total follow-up of 21 months. The relationships of plasma CTRP9 levels with the severity of coronary artery stenosis and adverse prognosis were assessed in patients with CAD. Compared with the mild lesion group, the CTRP9 was significantly lower in the moderate-severe lesion group. In the receiver-operating characteristics (ROC) curve analysis, a cut-off CTRP9 value of 266.95 ng/mL was identified for predicting moderate-severe lesions. A total of 97 MACEs (32.12%) were documented after 21 months of follow-up. Multivariable Cox regression analysis revealed that decreased plasma CTRP9 levels independently predicted MACEs (HR: 0.996, 95% CI: 0.994–0.998, P < 0.001) after adjustment for potential confounding factors. Kaplan–Meier survival curves illustrated a significantly higher incidence of MACEs in patients with decreased CTRP9 levels compared with those with higher levels. Plasma CTRP9 levels were associated with the severity of coronary artery disease. Lower plasma CTRP9 levels were indicative of moderate-severe coronary lesions and an increased risk of MACEs in patients with CAD.

Heart failure (HF) remains a significant global health concern with limited effective treatments available. C1q/TNF‐related protein 6 (CTRP6) is a member of the CTRP family analogous to adiponectin and its role in HF pathogenesis remains unclear. Here, we investigated the impact of CTRP6 on HF progression. To mimic heart failure with reduced ejection fraction (HFrEF), we used isoproterenol injection in mice and administered adenovirus vectors expressing CTRP6 (Ad‐CTRP6) via tail vein injection. We assessed cardiac function through echocardiography and histology. CTRP6's effects on hypertrophy, fibrosis, apoptosis, oxidative stress and mitochondrial function were analysed. Downstream pathways (phosphorylated AMP‐activated protein kinase (p‐AMPK), sirtuin 1 (SIRT1) and peroxisome proliferator‐activated receptor γ coactivator 1‐α (PGC‐1α) were studied in heart tissues. In vitro, isoproterenol‐stimulated H9c2 cardiomyocytes were treated with CTRP6 to examine viability, apoptosis, F‐actin and signalling proteins. Compound C was used to assess AMPK involvement. CTRP6 expression was lower in the plasma of HF patients. In an isoproterenol‐induced HFrEF mouse model, adenovirus‐mediated overexpression of CTRP6 ameliorated cardiac dysfunction and reduced cardiomyocyte apoptosis, oxidative stress, inflammation and myocardial injury markers. Mechanistically, CTRP6 activation of the AMPK/SIRT1/PGC‐1α signalling pathway restored mitochondrial homeostasis, evidenced by reduced mitochondrial reactive oxygen species levels, increased ATP content, and enhanced mitochondrial complex I/III activities in cardiac tissues. In vitro studies using isoproterenol‐stimulated H9c2 cardiomyocytes corroborated these findings, demonstrating that CTRP6 upregulation attenuated hypertrophy, apoptosis, oxidative stress and mitochondrial dysfunction. Furthermore, these effects were partially reversed by the AMPK inhibitor Compound C, implicating the involvement of the AMPK pathway in CTRP6‐mediated cardioprotection. CTRP6 alleviates HF progression through the AMPK/SIRT1/PGC‐1α signalling pathway. What is the central question of this study? What are the role and mechanisms of C1q/tumour necrosis factor‐related protein‐6 (CTRP6) in heart failure (HF) progression and its potential cardioprotective effects? What is the main finding and its importance? CTRP6 alleviates HF progression through the activation of the AMPK/SIRT1/PGC‐1α signalling pathway, reducing oxidative stress, inflammation and mitochondrial dysfunction. This may enable development of novel therapeutic strategies for HF management.

Background and aims Lipoprotein (a) [Lp(a)] is a genetically regulated lipoprotein particle that is an independent risk factor for coronary atherosclerotic heart disease. However, the correlation between Lp(a) and left ventricular ejection fraction (LVEF) in patients with myocardial infarction (MI) has been poorly studied. The present study investigated the correlation between Lp(a) and LVEF, as well as the impact of Lp(a) on long-term mortality in patients with MI. Methods Patients who underwent coronary angiography resulting in MI diagnosis between May 2018 and March 2020 at the First Affiliated Hospital of Anhui Medical University were included in this study. The patients were divided into groups based on the Lp(a) concentration and LVEF (reduced ejection fraction group: < 50%; normal ejection fraction group: ≥ 50%). Then, correlations between the Lp(a) level and LVEF, as well as the impact of Lp(a) on mortality, were assessed. Results This study included 436 patients with MI. The Lp(a) level and LVEF were significantly and negatively correlated (r = -0.407, β = -0.349, P  < 0.001). The area under the receiver operating characteristic curve (ROC) indicated that an Lp(a) concentration > 455 mg/L was the best predictive value for reduced ejection fraction (AUC: 0.7694, P  < 0.0001). The clinical endpoints did not differ based on the Lp(a) concentration. However, all-cause mortality and cardiac mortality differed based on LVEF. Conclusions These results suggest that an elevated Lp(a) concentration predicts reduced ejection fraction and that LVEF predicts all-cause mortality and cardiac mortality in patients with MI.

Background and aims Secreted frizzled-related protein 5 (SFRP5) is a member of the SFRP family that is known for its potent anti-inflammatory properties. Nevertheless, little is known regarding the relevance of SFRP5 in coronary artery disease (CAD). The current study examined the correlation between serum levels of SFRP5 and the triglyceride-glucose (TyG) index in patients who underwent coronary angiography (CAG) as a component of cardiovascular assessment and for the purpose of prognosis evaluation. Methods A total of 310 hospitalized patients were enrolled in this study between May 2021 and March 2022 and were divided into three groups based on their CAG results and SYNTAX (synergy between PCI with TAXUS drug-eluting stent and cardiac surgery) scores: the control group, mild lesion group, and moderate-severe lesion group. Univariate and multivariate analyses were employed to investigate the relationships between changes in patients and clinical variables. To investigate the impact of the TyG index and serum SFRP5 levels on the occurrence of major adverse cardiovascular events (MACEs), Kaplan‒Meier curves were plotted. Serum SFRP5 levels were measured utilizing an enzyme-linked immunosorbent assay (ELISA) kit. Results The serum SFRP5 levels significantly decreased with the increasing severity and complexity of CAD, while the TyG index significantly increased ( P  < 0.001). Moreover, a significant negative correlation was observed between the serum SFRP5 levels and the TyG index (r = -0.312, P  < 0.001). SFRP5 exerts a protective role in different groups of patients. The area under the receiver operating characteristic (ROC) curve indicated that an SFRP5 concentration > 115.58 pg/mL was the best predictive value for CAD (OR:0.87, P  < 0.001). MACEs were significantly associated with serum SFRP5 levels and the TyG index, as indicated by both univariate and multivariate Cox regression analyses ( P  < 0.001). Furthermore, Kaplan‒Meier analysis indicated that as the TyG index decreased and SFRP5 levels increased, the occurrence of MACEs decreased ( P  < 0.001). Patients with a concentration of SFRP5 > 115.58 pg/mL and a TyG index < 8.49 exhibited a better prognosis for avoiding MACEs ( P  < 0.001). Conclusion These results suggest that the collaboration between serum SFRP5 levels and the TyG index holds promise in predicting CAD and its prognosis.

Background and aims The prognostic relevance of Remnant cholesterol (RC) in acute myocardial infarction (AMI), particularly in diabetes mellitus (DM) patients, remains unclarified. This research aimed to explore the interaction between elevated RC and DM on the prognosis of AMI, with the goal of improving risk stratification and guiding intervention strategies. Methods In this retrospective, single-center study, 520 AMI patients were recruited. Basic and follow-up information was acquired, with the primary endpoint being major adverse cardiovascular events (MACE) and the secondary endpoint being cardiac mortality. Multiplicative and additive interactions were assessed to determine the combined impact of RC and DM on prognosis. Analytical methods included Cox regression, Kaplan–Meier survival, and ROC analyses. Results Over a median follow-up of 45 (42–49) months, 120 (23.08%) MACEs and 35 (6.73%) cardiac mortalities were observed. An additive interaction between elevated RC and DM was positively related to MACEs, with the attributable proportion suggesting that 62% of MACE risk could be attributed to this interaction. The synergy index was 3.46 for MACE, suggesting that the combined risk of both factors exceeded the sum of their individual risks. Multivariate Cox regression analysis identified RC as a significant predictor of both MACEs and cardiac death. Kaplan–Meier survival curves indicated an obvious increase in MACE when both high RC and DM were present (log-rank test, P  < 0.001). ROC analysis demonstrated that AUC for RC in estimating MACEs was higher in DM patients, reaching 0.676 (95% CI 0.567–0.786). Conclusions The combined presence of elevated RC and DM exerts a synergistic effect, providing valuable insights for the risk stratification of AMI patients.

The significance of uric acid (UA) and high-density lipoprotein cholesterol (HDL-C) in the prognosis of acute myocardial infarction (AMI) remains controversial. This study investigated the effect of the interaction between UA and HDL-C on the prognosis of patients with AMI. In total, 480 patients with AMI were included in this study. Baseline and follow-up data were collected, and the primary endpoint was major adverse cardiovascular events (MACE). The secondary endpoint was all-cause death. Both additive and multiplicative interactions were calculated to evaluate their interaction with prognosis. Then, the impact of UA and HDL-C ratio (UHR) on prognosis was assessed. Over a median follow-up period of 41 (30,46) months, 136 (28.3%) MACEs, and 44 (9.2%) deaths were recorded. There was a positive additive interaction between UA and HDL-C for MACEs. The attributable proportion (AP) showed that 46% of the estimated effect (MACE in patients) was attributable to this interaction. The synergy index (SI) was 2.04 (1.07,3.88) for MACE, indicating that the risk for patients presenting with both risk factors was greater than the sum of the risk factors alone. Multivariate Cox regression analysis revealed that UHR independently predicted MACEs and mortality. Kaplan-Meier survival curves according to tertiles of UHR showed statistically significant differences in MACE (log-rank test,  < 0.001). Receiver operating characteristic (ROC) analysis showed that the area under the curve (AUC) of UHR for predicting MACE was 0.716. The coexistence of high UA and low HDL-C has a synergistic effect and provides further information for risk stratification of patients with AMI. UHR is a simple and easily available prognostic indicator independent of traditional risk factors.

This study aimed to evaluate the diagnostic performance of combined dynamic stress CT myocardial perfusion imaging (CTP) and coronary CT angiography (CTA) alongside CT-derived fractional flow reserve (CT-FFR) in detecting hemodynamically significant coronary artery disease (CAD). A total of 33 patients (86 vessels) who underwent coronary CTA, dynamic stress CTP, and coronary angiography were included. Vessels exhibiting 30–90% stenosis were subjected to FFR analysis based on coronary angiography (Angio-FFR). Hemodynamic significance, determined by Angio-FFR ≤ 0.80, and imaging findings were evaluated. The evaluation involved a comparison between the combined use of coronary CTA, CTP and CT-FFR, versus the sole use of coronary CTA. Out of 86 coronary vessels, 17 (19.8%) exhibited hemodynamically significant stenosis. The sensitivity, specificity, and accuracy of coronary CTA for detecting ischemia were 94.12%, 34.78%, and 46.51%, respectively. Adding CTP to CTA improved specificity to 88.41%, and accuracy to 87.21%, respectively. The area under the curve (AUC) for the discrimination of functional significant stenosis was 0.798 when using CTA alone, and for CTA plus CTP, it reached 0.910. Furthermore, the combination of CTA, CTP and CT-FFR, showed accuracy of 88.37%, sensitivity of 88.24% and specificity of 88.41% with the AUC of 0.946. The integration of dynamic CTP with CTA significantly enhances the diagnostic accuracy for identifying patients with hemodynamically significant CAD, compared to the use of CTA alone. This study underscores the value of combining CTP, CT-FFR, and CTA in improving diagnostic precision for CAD. The combination of CTP, CT-FFR and CTA offers a multifaceted assessment for patients with CAD by simultaneously providing anatomical detail, functional analysis, and physiological quantification, which facilitating rapid, accurate, and optimal clinical decision-making and significantly enhances patient management.

Objective Long non-coding RNAs (lncRNAs) play critically in the pathogenesis of myocardial ischemia–reperfusion (I/R) injury. Thus, it was proposed to investigate the mechanism of LINC00461 in the disease through mediating microRNA-185-3p (miR-185-3p)/myeloid differentiation primary response gene 88 (Myd88) axis. Methods miR-185-3p, LINC00461 and Myd88 expression in mice with I/R injury was measured. Mice with I/R injury were injected with the gene expression-modified vectors, after which cardiac function, hemodynamics, myocardial enzyme, oxidative stress, and cardiomyocyte apoptosis were analyzed. Results I/R mice showed LINC00461 and Myd88 up-regulation and miR-185-3p down-regulation. Down-regulating LINC00461 or up-regulating miR-185-3p recovered cardiac function, reduced myocardial enzyme levels, and attenuated oxidative stress and cardiomyocyte apoptosis in mice with I/R. miR-185-3p overexpression rescued the promoting effect of LINC00461 upregulation on myocardial injury in I/R mice. Conclusion LINC00461 knockdown attenuates myocardial I/R injury via elevating miR-185-3p expression to suppress Myd88 expression.