Dipicolylamine Derivatives Bearing Pyrene and Anthracene as Molecular Probes for Cu and HS.

Two dipicolylamine (DPA) derivatives with the pyrene and anthracene groups, 1-(pyren-1-yl)-N, N-bis-(pyridine-2-ylmethyl)benzylamine (L1) and 1-(anthracen-9-yl)-N, N-bis-(pyridine-2-ylmethyl)benzylamine (L2) were synthesized, characterized, and their affinitive properties for metal ions were studied. The mass spectroscopy and Job's plots showed that L1 and L2 reacted with Cu and formed complexes [Cu(L1)(solvent)] (L1-Cu) and [Cu(L2)(solvent)] (L2-Cu), respectively. Both L1 and L2 were fluorescent probes recognizing Cu via the emission quenching and further detecting HS via the emission revival.

Investigation of autophagy‑related genes and immune infiltration in calcific aortic valve disease: A bioinformatics analysis and experimental validation.

The present study aimed to elucidate the role of autophagy-related genes (ARGs) in calcific aortic valve disease (CAVD) and their potential interactions with immune infiltration via experimental verification and bioinformatics analysis. A total of three microarray datasets (GSE12644, GSE51472 and GSE77287) were obtained from the Gene Expression Omnibus database, and gene set enrichment analysis was performed to identify the relationship between autophagy and CAVD. After differentially expressed genes and differentially expressed ARGs (DEARGs) were identified using CAVD samples and normal aortic valve samples, a functional analysis was performed, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses, protein-protein interaction network construction, hub gene identification and validation, immune infiltration and drug prediction.

Resveratrol protects cardiomyocytes against ischemia/reperfusion-induced ferroptosis via inhibition of the VDAC1/GPX4 pathway.

The present study aimed to explore how resveratrol (Res) confers myocardial protection by attenuating ferroptosis. In vivo and in vitro myocardial ischemia/reperfusion injury (MIRI) models were established, with or without Res pretreatment. The results showed that Res pretreatment effectively attenuated MIRI, as evidenced by increased cell viability, reduced lactate dehydrogenase activity, decreased infarct size, and maintained cardiac function.

Role of dysregulated ferroptosis‑related genes in cardiomyocyte ischemia‑reperfusion injury: Experimental verification and bioinformatics analysis.

Acute myocardial infarction is a life-threatening condition with high mortality and complication rates. Although myocardial reperfusion can preserve ischemic myocardial tissue, it frequently exacerbates tissue injury, a phenomenon known as ischemia-reperfusion injury (IRI). However, the underlying pathological mechanisms of IRI remain to be completely understood.

Tanshinone IIA confers protection against myocardial ischemia/reperfusion injury by inhibiting ferroptosis and apoptosis via VDAC1.

Tanshinone IIA (TSN) extracted from danshen () could protect cardiomyocytes against myocardial ischemia/reperfusion injury (IRI), however the underlying molecular mechanisms of action remain unclear. The aim of the present study was to identify the protective effects of TSN and its mechanisms of action through studies. An anoxia/reoxygenation (A/R) injury model was established using H9c2 cells to simulate myocardial IRI .

NSD2 promotes pressure overload-induced cardiac hypertrophy via activating circCmiss1/TfR1/ferroptosis signaling.

Heart failure typically occurs early in the clinical course of sustained cardiac hypertrophy that is accompanied by maladaptive remodeling of the heart. It is critical to discover new mechanisms and effective therapeutic targets to prevent and cure pathological cardiac hypertrophy. The objective of the study was to evaluate the effects of circRNAs on NSD2-induced ventricular remodeling.

Exploring Dysregulated Ferroptosis-Related Genes in Septic Myocardial Injury Based on Human Heart Transcriptomes: Evidence and New Insights.

Introduction: Sepsis is currently a common condition in emergency and intensive care units, and is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Cardiac dysfunction caused by septic myocardial injury (SMI) is associated with adverse prognosis and has significant economic and human costs. The pathophysiological mechanisms underlying SMI have long been a subject of interest.

Assessing the impact of blocking distal coronary sinus-left atrial muscular connection on inducible rate of atrial fibrillation and follow-up recurrence in persistent atrial fibrillation patients with different fibrotic degrees of left atrial: A retrospective study.

Background: The musculature of the coronary sinus (CS), especially its distal connection with the post wall of the left atrial (LA), has been associated with the genesis and maintenance of atrial flutter (AFL) and atrial fibrillation (AF). However, the relative contributions of the distal coronary sinus (CSD)-LA connection to PersAF with various degrees of atrial fibrosis remain unknown.

Objective: This study aimed to explore the different roles of blocking the CSD-LA connection in the induction of acute AF and middle-term follow-up of recurrence among PersAF patients with various degrees of LA fibrosis.

Dysregulated autophagy-related genes in septic cardiomyopathy: Comprehensive bioinformatics analysis based on the human transcriptomes and experimental validation.

Septic cardiomyopathy (SCM) is severe organ dysfunction caused by sepsis that is associated with poor prognosis, and its pathobiological mechanisms remain unclear. Autophagy is a biological process that has recently been focused on SCM, yet the current understanding of the role of dysregulated autophagy in the pathogenesis of SCM remains limited and uncertain. Exploring the molecular mechanisms of disease based on the transcriptomes of human pathological samples may bring the closest insights.

Identification and Validation of Ferroptosis-Related Biomarkers in Septic Cardiomyopathy via Bioinformatics Analysis.

Septic cardiomyopathy (SCM) is a cardiac dysfunction caused by severe sepsis and septic shock that increases the risk of heart failure and death and its molecular mechanism remains unclear. Ferroptosis, a novel form of programmed cell death, has been reported to be present in the heart tissue of patients with sepsis, which demonstrated that ferroptosis may be a potential mechanism of myocardial injury in SCM. Therefore, we explored the role of ferroptosis-related genes (FRGs) in SCM and aimed to identify pivotal ferroptosis-related targets in SCM and potential therapeutic targets involved in the pathological process of SCM.

Keap-NRF2 signaling contributes to the Notch1 protected heart against ischemic reperfusion injury via regulating mitochondrial ROS generation and bioenergetics.

Myocardial ischemia/reperfusion (I/R) injury is recognized as the leading cause of death worldwide. However, the molecular mechanisms involved in this process are still not fully understood. We previously reported that the combined action of Notch1 and Keap1-NRF2 signaling pathway can significantly increase the activity of cardiomyocytes, inhibit the apoptosis of cardiomyocytes, reduce the formation of reactive oxygen species, and improve the antioxidant activity in neonate rat myocardial cells.

ITGB1-DT/ARNTL2 axis may be a novel biomarker in lung adenocarcinoma: a bioinformatics analysis and experimental validation.

Background: Lung cancer is one of the most lethal malignant tumors that endangers human health. Lung adenocarcinoma (LUAD) has increased dramatically in recent decades, accounting for nearly 40% of all lung cancer cases. Increasing evidence points to the importance of the competitive endogenous RNA (ceRNA) intrinsic mechanism in various human cancers.

Plasma Lipidomics Identifies Unique Lipid Signatures and Potential Biomarkers for Patients With Aortic Dissection.

Aortic dissection (AD) is a catastrophic cardiovascular emergency with a poor prognosis, and little preceding symptoms. Abnormal lipid metabolism is closely related to the pathogenesis of AD. However, comprehensive lipid alterations related to AD pathogenesis remain unclear.

Iron Metabolism and Idiopathic Pulmonary Arterial Hypertension: New Insights from Bioinformatic Analysis.

Idiopathic pulmonary arterial hypertension (IPAH) is a rare vascular disease with a poor prognosis, and the mechanism of its development remains unclear. Further molecular pathology studies may contribute to a comprehensive understanding of IPAH and provide new insights into diagnostic markers and potential therapeutic targets. Iron deficiency has been reported in 43-63% of patients with IPAH and is associated with reduced exercise capacity and higher mortality, suggesting that dysregulated iron metabolism may play an unrecognized role in influencing the development of IPAH.

Role of ferroptosis-related genes in Stanford type a aortic dissection and identification of key genes: new insights from bioinformatic analysis.

Stanford type A aortic dissection (TAAD) is one of the most dangerous vascular diseases worldwide, and the mechanisms of its development remain unclear. Further molecular pathology studies may contribute to a comprehensive understanding of TAAD and provide new insights into diagnostic markers and potential therapeutic targets. Recent studies have identified that ferroptosis, a form of cell death, may play a previously unrecognized role in influencing the development of TAAD.

LncRNA SNHG12 regulates the miR-101-3p/CUL4B axis to mediate the proliferation, migration and invasion of non-small cell lung cancer.

Mounting evidence has shown that long noncoding RNAs (lncRNAs) play critical roles in carcinogenesis and tumor progression. SNHG12 has been identified in multiple types of malignant tumors. However, the role of SNHG12 in human non-small cell lung cancer (NSCLC) is poorly characterized, and the relevant underlying mechanism remains unclear.

Curcumin protects cardiomyopathy damage through inhibiting the production of reactive oxygen species in type 2 diabetic mice.

Type 2 diabetes mellitus (DM)-induced cardiomyopathy is a multifactorial and complex disease involving oxidative stress, lipids, and fibrosis. It is based on metabolic disorders and microvascular disease and causes extensive focal necrosis of the heart muscle. Curcumin (CUR) is a natural polyphenol isolated from turmeric rhizomes and plays an important role in the antioxidant, anti-apoptotic and anti-inflammatory effects of diabetes.

Inorganic phosphate-osteogenic induction medium promotes osteogenic differentiation of valvular interstitial cells via the BMP-2/Smad1/5/9 and RhoA/ROCK-1 signaling pathways.

Calcific aortic valve disease (CAVD) currently lacks a highly effective model. The presence of high concentrations of serum inorganic phosphate in patients with end-stage renal disease leads to calcification of vascular and aortic valves. Therefore, we applied inorganic phosphate to induce the osteogenic differentiation of valvular interstitial cells (VICs) and mimic its pathophysiological effects.

[Corrigendum] Hypoxia‑induced internalization of connexin 26 and connexin 43 in pulmonary epithelial cells is involved in the occurrence of non‑small cell lung cancer via the P53/MDM2 signaling pathway.

Following the publication of this article, the authors have realized that the corrsesponding author's name was printed incorrectly in the journal: This was mispelled as "Jin Zhou". The corrected name (Jing Zhou) is printed above. The authors regret any inconvenience this has caused, and thank the Editor for allowing them the opportunity to publish a Corrigendum.

Alveolar adenoma with poor imaging: a case report.

Alveolar adenoma is an isolated, well-defined peripheral lung tumor that originates from type II alveolar cells. The tumor consists of a network of simple, low-cubic, epithelium-coated lacunae with varying amounts of fine and inconspicuous-to-thick spindle cells that sometimes contain mucus sample matrix. Few cases of alveolar adenoma have been reported.

Hypoxia‑induced internalization of connexin 26 and connexin 43 in pulmonary epithelial cells is involved in the occurrence of non‑small cell lung cancer via the P53/MDM2 signaling pathway.

Reports have highlighted an association between connexins (CXs) or gap junction proteins and non‑small cell lung cancer (NSCLC). In the present study, it was aimed to elucidate the regulatory mechanism of CX26 and CX43 under hypoxic conditions in NSCLC. Clinical samples were collected for analysis of CX26 and CX43 expression and clinical cancerization followed by quantification of CX26 and CX43 expression.