An innovative viewpoint on the existing and prospectiveness of SR-B1.

Scavenger Receptor Class B Type 1 (SR-B1), a receptor protein expressed on the cell membrane, plays a crucial role in the metabolism and transport of cholesterol and other lipids, contributing significantly to the homeostasis of lipid levels within the body. Bibliometric analysis involves the application of mathematical and statistical methods to quantitatively analyze different types of documents. It involves the analysis of structural and temporal trends in scholarly articles, coupled with the identification of subject emphasis and variations. Through a bibliometric analysis, this study examines the historical background, current research trends, and future directions in the exploration of SR-B1. By offering insights into the research status and development of SR-B1, this paper aims to assist researchers in identifying novel pathways and areas of investigation in this field of study. Following the screening process, it can be concluded that research on SR-B1 has consistently remained a topic of significant interest over the past 17 years. Interestingly, SR-B1 has recently garnered attention in areas beyond its traditional research focus, including the field of cancer. The primary objective of this review is to provide a concise and accessible overview of the development process of SR-B1 that can help readers who are not well-versed in SR-B1 research quickly grasp its key aspects. Furthermore, this review aims to offer insights and suggestions to researchers regarding potential future research directions and areas of emphasis relating to SR-B1.

A new perspective on the current and future development potential of ABCG1.

ABCG1 is an essential protein involved in the efflux of intracellular cholesterol to the extracellular space, thus playing a critical role in reducing cholesterol accumulation in neighboring tissues. Bibliometric analysis pertains to the interdisciplinary field of quantitative examination of diverse documents using mathematical and statistical techniques. It integrates the investigation of structural and temporal patterns in academic publications with an exploration of subject focus and forms of uncertainty. This research paper examines the historical evolution, current areas of interest, and future development trends of ABCG1 through bibliometric analysis. This study aims to offer readers insights into the research status and emerging trends of ABCG1, thereby assisting researchers in the exciting field to explore novel research avenues. Following rigorous selection, research on ABCG1 has remained highly active over the past two decades. ABCG1 has even started to emerge in previously unrelated fields, such as the field of cancer research. According to the analysis conducted by Citespace, a lot of keywords and influential citations were identified. ABCG1 has been found to establish a connection between cancer and cardiovascular disease, highlighting their interrelationship. This review aims to assist readers who have limited familiarity with ABCG1 research in gaining a rapid understanding of its developmental trajectory. Additionally, it aims to offer researchers potential areas of focus for future studies related to ABCG1.

The Potential Relationship Between Cardiovascular Diseases and Monkeypox.

Mpox, a novel epidemic disease, has broken out the period of coronavirus disease 2019 since May 2022, which was caused by the mpox virus. Up to 12 September 2023, there are more than 90,439 confirmed mpox cases in over 115 countries all over the world. Moreover, the outbreak of mpox in 2022 was verified to be Clade II rather than Clade I. Highlighting the significance of this finding, a growing body of literature suggests that mpox may lead to a series of cardiovascular complications, including myocarditis and pericarditis. It is indeed crucial to acquire more knowledge about mpox from a perspective from the clinical cardiologist. In this review, we would discuss the epidemiological characteristics and primary treatments of mpox to attempt to provide a framework for cardiovascular physicians.

Apelin-13: A Protective Role in Vascular Diseases.

Vascular disease is a common problem with high mortality all over the world. Apelin-13, a key subtype of apelin, takes part in many physiological and pathological responses via regulating many target genes and target molecules or participating in many signaling pathways. More and more studies have demonstrated that apelin-13 is implicated in the onset and progression of vascular disease in recent years. It has been shown that apelin-13 could ameliorate vascular disease by inhibiting inflammation, restraining apoptosis, suppressing oxidative stress, and facilitating autophagy. In this article, we sum up the progress of apelin-13 in the occurrence and development of vascular disease and offer some insightful views about the treatment and prevention strategies of vascular disease.

A Potential Role of NFIL3 in Atherosclerosis.

Nuclear factor interleukin-3 (NFIL3), a proline- and acidic-residue-rich (PAR) bZIP transcription factor, is called the E4 binding protein 4 (E4BP4) as well, which is relevant to regulate the circadian rhythms and the viability of cells. More and more evidence has shown that NFIL3 is associated with different cardiovascular diseases. In recent years, it has been found that NFIL3 has significant functions in the progression of atherosclerosis (AS) via the regulation of inflammatory response, macrophage polarization, some immune cells and lipid metabolism. In this overview, we sum up the function of NFIL3 during the development of AS and offer meaningful views how to treat cardiovascular disease related to AS.

Leucine zipper protein 1 attenuates pressure overload-induced cardiac hypertrophy through inhibiting Stat3 signaling.

INTRODUCTION: Cardiac hypertrophy is an important contributor of heart failure, and the mechanisms remain unclear. Leucine zipper protein 1 (LUZP1) is essential for the development and function of cardiovascular system; however, its role in cardiac hypertrophy is elusive. OBJECTIVES: This study aims to investigate the molecular basis of LUZP1 in cardiac hypertrophy and to provide a rational therapeutic approach. METHODS: Cardiac-specific Luzp1 knockout (cKO) and transgenic mice were established, and transverse aortic constriction (TAC) was used to induce pressure overload-induced cardiac hypertrophy. The possible molecular basis of LUZP1 in regulating cardiac hypertrophy was determined by transcriptome analysis. Neonatal rat cardiomyocytes were cultured to elucidate the role and mechanism of LUZP1 in vitro. RESULTS: LUZP1 expression was progressively increased in hypertrophic hearts after TAC surgery. Gain- and loss-of-function methods revealed that cardiac-specific LUZP1 deficiency aggravated, while cardiac-specific LUZP1 overexpression attenuated pressure overload-elicited hypertrophic growth and cardiac dysfunction in vivo and in vitro. Mechanistically, the transcriptome data identified Stat3 pathway as a key downstream target of LUZP1 in regulating pathological cardiac hypertrophy. Cardiac-specific Stat3 deletion abolished the pro-hypertrophic role in LUZP1 cKO mice after TAC surgery. Further findings suggested that LUZP1 elevated the expression of Src homology region 2 domain-containing phosphatase 1 (SHP1) to inactivate Stat3 pathway, and SHP1 silence blocked the anti-hypertrophic effects of LUZP1 in vivo and in vitro. CONCLUSION: We demonstrate that LUZP1 attenuates pressure overload-induced cardiac hypertrophy through inhibiting Stat3 signaling, and targeting LUZP1 may develop novel approaches to treat pathological cardiac hypertrophy.

Nesfatin-1, a novel energy-regulating peptide, alleviates pulmonary fibrosis by blocking TGF-ß1/Smad pathway in an AMPKα-dependent manner.

Pulmonary fibrosis is a chronic progressive disease which steadily causes a critical public health concern. Nesfatin-1, a novel energy-regulating peptide discovered in 2006, could increase the level of AMPK phosphorylation. Previous studies have unveiled that Nesfatin-1 possessed many pharmacological effects including anti-inflammation, anti-oxidative stress, anti-fibrosis, and the regulation of lipid metabolism. Here, we investigated the impact of Nesfatin-1 on pulmonary fibrosis. Male C57BL/6J mice were intraperitoneally injected with Nesfatin-1 (10 µg·kg-1·day-1) for 21 days since mice were intratracheally administrated with bleomycin (BLM) (2 U/kg). Primary murine lung fibroblasts were stimulated with TGF-ß1 (10 ng/ml) for 48 h. The results showed that Nesfatin-1 treatment significantly improved pulmonary function and decreased the production of collagen in BLM-treated mice. Meantime, Nesfatin-1 treatment also inhibited oxidative stress and inflammation in lung tissues from BLM-treated mice. Mechanically, Nesfatin-1 blocked the activation of TGF-ß1/Smad2/3 signaling pathway in lung tissues challenged with BLM. In addition, we found that Nesfatin-1 enhanced the phosphorylation of AMPKα during pulmonary fibrosis. However, pharmacological inhibition or genetic deletion of AMPKα could both offset the pulmonary protection mediated by Nesfatin-1 during pulmonary fibrosis. Our experimental results firstly show Nesfatin-1 might serve as a novel treatment or adjuvant against pulmonary fibrosis by blocking TGF-ß1/Smad pathway in an AMPKα-dependent manner.

Introduction and comparision of three different fixation methods in the suprahepatic space in laparoscopy-assisted ventriculoperitoneal shunt for hydrocephalus.

Ventriculoperitoneal shunt (VPS) placement is the standard procedure in the management of hydrocephalus. The introduction of laparoscopy allows better visualization during the operation and a more reliable placement of the peritoneal terminal of the catheter, which significantly decreases postoperative obstruction and malposition rates. However, the fixation methods of the peritoneal terminal of the catheter have not been previously discussed. The indications, techniques, and complications were compared between conventional VPS and laparoscopy-guided VPS. Furthermore, same analyses were performed within the laparoscopy-guided VPS group subdivided by three different techniques of the fixation of the peritoneal terminal of catheter, including suture and ligature, titanium clip fixation, and subcutaneous fixation. A total of 137 patients with hydrocephalus who received VPS treatment was retrospectively studied, 85 of which were laparoscopy-guided, and 52 were not. The distal ends of the catheters were all placed in the suprahepatic space. At least one year (mean 28.6 months) follow-up was given postoperatively. The average duration of the whole operation was 45 min for suture and ligature, 40 min for titanium clip fixation, and 30 min for the subcutaneous fixation, respectively. Six patients (4.4%) had obstructive of the ventricular catheter in total. The success rates for the laparoscopy-assisted VPS procedure and the conventional VPS procedure were 87.1% (74/85) and 80.8% (42/52), respectively. Within subgroups of the laparoscopy-assisted VPS divided by fixation methods, the procedures were successful in 85.2% (23/27) of suture and ligation, 82.1% (23/28) of titanium clip fixation, and 93.3% (28/30) of subcutaneous fixation, respectively. Two patients had dislocated shunt tube in peritoneal end in laparoscopy group, all in the titanium clip fixation subgroups. The laparoscopy-assisted VPS insertion is an ideal shunt method for its effectiveness and lesser complication rate after operation. The subcutaneous fixation method of the peritoneal terminal of catheter might be the optimal fixation technique.

Hepatocyte-derived exosomes deliver H2AFJ to hepatic stellate cells and promote liver fibrosis via the MAPK/STMN1 axis activation.

Hepatic stellate cells (HSCs) activate and acquire proliferative features in response to liver injury. However, mechanisms involved in the activation of fibrotic HSCs remain uncharacterized. This study aims at elaborating the mechanistic basis by which exosomal H2AFJ derived from hepatocytes might affect the activation of HSCs and liver fibrosis. Bioinformatics analysis based on transcriptomic RNA-seq data was used to screen out the downstream regulatory genes and pathways of H2AFJ. Mouse hepatocytes AML-12 cells were stimulated with CCl4 to mimic an in vitro microenvironment of liver fibrosis, from which exosomes were isolated. Next, HSCs were co-cultured with hepatocyte-derived exosomes followed by detection of HSC migration and invasion in the presence of manipulated H2AFJ and STMN1 expression and MAPK pathway inhibitor. It was found that H2AFJ was highly expressed in hepatocyte-derived exosomes after CCl4 stimulation. Hepatocyte-derived exosomal H2AFJ promoted HSC migration and invasion. H2AFJ upregulated c-jun-mediated STMN1 by activating the MAPK signaling pathway. Furthermore, in vivo experiments verified that silencing of H2AFJ attenuated liver fibrosis in mice, while restoration of STMN1 negated its effect. Collectively, hepatocyte-derived exosomal H2AFJ aggravated liver fibrosis by activating the MAPK/STMN1 signaling pathway. This study provides a potential therapeutic target for alleviating liver fibrosis.

Visual assessment and quantitative analysis of bone marrow edema in young and middle-aged versus elderly patients with vertebral compression fracture by spectral CT.

BACKGROUND: For the diagnosis of bone marrow edema (BME), spectral computed tomography (CT) has emerged as a promising technique. PURPOSE: To study the different performances of spectral CT in the diagnosis of vertebral BME in young and middle-aged versus elderly patients. MATERIAL AND METHODS: Magnetic resonance imaging (MRI) was used as the gold standard. To determine the existence of BME, spectral CT color-coded images of the vertebral bodies of 82 patients with vertebral compression fractures (VCFs) were visually inspected. A quantitative analysis of the spectral CT vertebral water concentration in the diagnosis of BME was performed using a receiver operating characteristic (ROC) curve. Patients were divided into two groups for comparison: the young and middle-aged group; and the elderly group. RESULTS: The sensitivity and specificity for visual assessment were 83.7% and 98.3%, respectively, in the young and middle-aged group and 96.8% and 98.2%, respectively, in the elderly group. The elderly group had a higher sensitivity than the young and middle-aged group (P < 0.05). With a threshold of 1046.2 mg/cm3, the ROC curve for the young and middle-aged group displayed an area under the curve (AUC) of 0.870, sensitivity of 86.0%, and specificity of 81.4%. The threshold of 1031.4 mg/cm3 yielded a sensitivity of 95.2% and a specificity of 98.4%, and the AUC of the elderly group was 0.997. The elderly group had a higher level of specificity than the young and middle-aged group (P < 0.05). CONCLUSION: Spectral CT can reliably diagnose BME in VCFs, and it performs better in elderly people than in young and middle-aged people.

Macrophage Sprouty4 deficiency diminishes sepsis-induced acute lung injury in mice.

OBJECTIVE: Inflammation and oxidative stress play critical roles in sepsis-induced acute lung injury (ALI). Sprout4 (Spry4) is involved in regulating inflammation and tissue injury; however, its role and mechanism in sepsis-induced ALI remain elusive. METHODS: Macrophage-specific Spry4 knockout (Spry4MKO), transgenic (Spry4MTG) mice and matched control littermates were generated and exposed to cecum ligation and puncture (CLP) surgery to establish bacterial sepsis-induced ALI. Bone marrow-derived macrophages (BMDMs) from Spry4MKO or Spry4MTG mice were isolated and subjected to lipopolysaccharide (LPS) stimulation to further validate the role of Spry4 in vitro. To verify the necessity of AMP-activated protein kinase (AMPK), Spry4 and AMPK double knockout mice and compound C were used in vivo and in vitro. BMDMs were treated with STO-609 to inhibit calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2). RESULTS: We found that macrophage Spry4 was increased in CLP mice and positively correlated with sepsis-induced ALI. Macrophage Spry4 deficiency prevented, while macrophage Spry4 overexpression exacerbated sepsis-induced inflammation, oxidative stress and ALI in mice and BMDMs. Mechanistic studies revealed that macrophage Spry4 deficiency alleviated sepsis-induced ALI through activating CaMKK2/AMPK pathway. CONCLUSION: Our study identify macrophage Spry4 as a promising predictive and therapeutic target of sepsis-induced ALI.

TRIM7 modulates NCOA4-mediated ferritinophagy and ferroptosis in glioblastoma cells.

OBJECTIVE: Glioblastoma is one of the most common intracranial malignant tumors with an unfavorable prognosis, and iron metabolism as well as ferroptosis are implicated in the pathogenesis of glioblastoma. The present study aims to decipher the role and mechanisms of tripartite motif-containing protein 7 (TRIM7) in ferroptosis and glioblastoma progression. METHODS: Stable TRIM7-deficient or overexpressing human glioblastoma cells were generated with lentiviral vectors, and cell survival, lipid peroxidation and iron metabolism were evaluated. Immunoprecipitation, protein degradation and ubiquitination assays were performed to demonstrate the regulation of TRIM7 on its candidate proteins. RESULTS: TRIM7 expression was elevated in human glioblastoma cells and tissues. TRIM7 silence suppressed growth and induced death, while TRIM7 overexpression facilitated growth and inhibited death of human glioblastoma cells. Meanwhile, TRIM7-silenced cells exhibited increased iron accumulation, lipid peroxidation and ferroptosis, which were significantly reduced by TRIM7 overexpression. Mechanistically, TRIM7 directly bound to and ubiquitinated nuclear receptor coactivator 4 (NCOA4) using K48-linked chains, thereby reducing NCOA4-mediated ferritinophagy and ferroptosis of human glioblastoma cells. Moreover, we found that TRIM7 deletion sensitized human glioblastoma cells to temozolomide therapy. CONCLUSION: We for the first time demonstrate that TRIM7 modulates NCOA4-mediated ferritinophagy and ferroptosis in glioblastoma cells, and our findings provide a novel insight into the progression and treatment for human glioblastoma.

The Application of Two-Stage Operation for High-Risk Patients with Oesophageal Cancer Following Gastrectomy.

BACKGROUND: Oesophageal replacement by colonic interposition remains a major challenge due to its complexity and high incidence of complications; here we applied the two-stage operation strategy to oesophageal replacement by colonic interposition in high-risk oesophageal cancer patients following gastrectomy. METHODS: We performed a retrospective analysis on the data of patients with a history of distal gastrectomy who underwent one-stage and two-stage oesophageal replacement by colonic interposition from February 2012 to February 2020, and explored the relationship between the staging strategy and postoperative outcomes. RESULTS: The clinical data of 93 patients were collected and analysed. There were no significant differences in the patients' characteristics between the two groups (all p > 0.05), except for comorbidities and Charlson Comorbidity Index (all p < 0.05). The Clavien-Dindo score between the two groups was also not significantly different (p > 0.05). The logistic regression models revealed that patients who had received preoperative therapy had a higher Clavien-Dindo score (p < 0.05), but the stage strategy did not (p > 0.05). CONCLUSIONS: The two-stage operation is feasible in high-risk patients who need to undergo colonic interposition for oesophageal replacement. At the same time, it lowers the technical threshold of colonic interposition for oesophageal replacement, increasing this surgical technique's acceptability.

Accuracy and sensitivity of high mobility group box 1 (HMGB1) in diagnosis of acute kidney injury caused by sepsis and relevance to prognosis.

OBJECTIVE: The diagnostic value of high mobility group box 1 (HMGB1) levels in patients with acute kidney injury (AKI) caused by sepsis and its relationship with disease prognosis were investigated to improve patient survival. METHODS: A total of 120 patients diagnosed with sepsis by comprehensive clinical examination were selected as the research subjects. According to the presence or absence of concurrent AKI, all patients were divided into SIAKI (50 cases with concurrent AKI) and N-AKI groups (70 cases without concurrent AKI). Sixty normal people receiving a physical examination in our hospital during the same period were divided into the control group. The diagnostic efficacy and the influences of HMGB1 on prognosis were assessed. RESULTS: HMGB1 levels in the serum and urine of the control group (3.43 ± 0.73 pg/mL, 343.13 ± 51.03 pg/mL) were both lower than those of the SIAKI (14.76 ± 2.44 pg/mL, 1109.76 ± 225.66 pg/mL) and N-AKI groups (7.99 ± 1.84 pg/mL, 890.54 ± 97.76 pg/mL) (P < 0.05). HMGB1 in the serum of the SIAKI group was higher than that of the N-AKI group (P < 0.05). The sensitivity (88%), specificity (87%), accuracy (88%), and area under the curve (AUC) (0.891) of the joint diagnosis of HMGB1 in blood and urine were superior to the diagnostic effects of HMGB1 in serum (70%, 70%, 70%, and 0.701) and HMGB1 in urine (59%, 57%, 58%, and 0.677) (P < 0.05). The proportion of HMGB1 in the nonsurvivors was higher than that in the survivors (85%) and was obviously higher than that in the survivors (15%) (P < 0.05). CONCLUSION: As a diagnostic marker of sepsis complicated with AKI, HMGB1 in serum and urine showed good application value. Serum HMGB1 could be used to assess disease prognosis with good clinical promotion.

Macrophage SAMSN1 protects against sepsis-induced acute lung injury in mice.

OBJECTIVE: Inflammation and oxidative stress contribute to the progression of sepsis-induced acute lung injury (ALI). SAM domain, SH3 domain and nuclear localization signals 1 (SAMSN1) is a signaling adaptor protein, and mainly regulates inflammatory response of various immune cells. The present study generates macrophage-specific SAMSN1-knockout (Samsn1MKO) and SAMSN1-transgenic (Samsn1MTG) mice to investigate its role and mechanism in sepsis-induced ALI. METHODS: Samsn1MKO and Samsn1MTG mice were exposed to lipopolysaccharide (LPS) instillation or cecal ligation and puncture (CLP) surgery to induce sepsis-induced ALI. Bone marrow transplantation, cellular depletion and non-invasive adoptive transfer of bone marrow-derived macrophages (BMDMs) were performed to validate the role of macrophage SAMSN1 in sepsis-induced ALI in vivo. Meanwhile, BMDMs were isolated from Samsn1MKO or Samsn1MTG mice to further clarify the role of SAMSN1 in vitro. RESULTS: Macrophage SAMSN1 expression was increased in response to LPS stimulation, and negatively correlated with LPS-induced ALI in mice. Macrophage SAMSN1 deficiency exacerbated, while macrophage SAMSN1 overexpression ameliorated LPS-induced inflammation, oxidative stress and ALI in mice and in BMDMs. Mechanistically, we found that macrophage SAMSN1 overexpression prevented LPS-induced ALI though activating AMP-activated protein kinase α2 (AMPKα2) in vivo and in vitro. Further studies revealed that SAMSN1 directly bound to growth factor receptor bound protein 2-associated protein 1 (GAB1) to prevent its protein degradation, and subsequently enhanced protein kinase A (PKA)/AMPKα2 activation in a protein tyrosine phosphatase, non-receptor type 11 (PTPN11, also known as SHP2)-dependent manner. Moreover, we observed that macrophage SAMSN1 overexpression diminished CLP-induced ALI in mice. CONCLUSION: Our study documents the protective role of macrophage SAMSN1 against sepsis-induced inflammation, oxidative stress and ALI through activating AMPKα2 in a GAB1/SHP2/PKA pathway, and defines it as a promising biomarker and therapeutic target to treat sepsis-induced ALI.