Publications by authors named "Liujun Jiang"

Aortic aneurysm is a life-threatening disease caused by progressive dilation of the aorta and weakened aortic walls. Its pathogenesis involves an imbalance between connective tissue repair and degradation. CD34 cells comprise a heterogeneous population that exhibits stem cell and progenitor cell properties.

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Endothelial cell (EC) damage or dysfunction serves as the initial event in the pathogenesis of various cardiovascular diseases. Progenitor cells have been postulated to be able to differentiate into ECs, facilitate endothelial regeneration, and alleviate vascular pathological remodeling. However, the precise cellular origins and underlying mechanisms remain elusive.

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Vascular inflammation and endothelial dysfunction contribute to vascular diseases. While neutrophil extracellular traps (NETs) participate in some vascular pathologies, their roles in lower limb ischemia remain poorly defined. This study investigated the functional significance of NETs in vascular inflammation and remodeling associated with limb ischemia.

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Background And Aims: Coronary small vessel disease (CSVD) is often associated with significant percutaneous coronary intervention (PCI) related complications, complex lesions, complex PCI, and poor long-term prognosis. We designed this retrospective study to clarify the characteristics, risk factors, and prognostic analyses of CSVD in Chinese populations.

Methods: A total of 986 patients who underwent coronary angiography and stent implantation at the First Affiliated Hospital of Zhejiang University School of Medicine were evaluated.

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The ambiguous results of multiple CD34 cell-based therapeutic trials for patients with heart disease have halted the large-scale application of stem/progenitor cell treatment. This study aimed to delineate the biological functions of heterogenous CD34 cell populations and investigate the net effect of CD34 cell intervention on cardiac remodeling. We confirmed, by combining single-cell RNA sequencing on human and mouse ischemic hearts and an inducible Cd34 lineage-tracing mouse model, that Cd34 cells mainly contributed to the commitment of mesenchymal cells, endothelial cells (ECs), and monocytes/macrophages during heart remodeling with distinct pathological functions.

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Regeneration of smooth muscle cells (SMCs) is vital in vascular remodeling. Sca1 stem/progenitor cells (SPCs) can generate de novo smooth muscle cells after severe vascular injury during vessel repair and regeneration. However, the underlying mechanisms have not been conclusively determined.

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Background: CD34 cells have been used to treat the patients with heart failure, but the outcome is variable. It is of great significance to scrutinize the fate and the mechanism of CD34 cell differentiation in vivo during heart failure and explore its intervention strategy.

Methods: We performed single-cell RNA sequencing (scRNA-seq) of the total non-cardiomyocytes and enriched Cd34-tdTomato lineage cells in the murine (male Cd34-CreERT2; Rosa26-tdTomato mice) pressure overload model (transverse aortic constriction, TAC), and total non-cardiomyocytes from human adult hearts.

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Background: Transplant arteriosclerosis is a major complication in long-term survivors of heart transplantation. Increased lymph flow from donor heart to host lymph nodes has been reported to play a role in transplant arteriosclerosis, but how lymphangiogenesis affects this process is unknown.

Methods: Vascular allografts were transplanted among various combinations of mice, including wild-type, -CreER;R26-tdTomato, -Cre-tdTomato, severe combined immune deficiency, , , and / mice.

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Background: Post-stroke spasticity is a cause of gait dysfunction and disability. Focal vibration (FV) of agonist-antagonist upper limb muscle pairs reduces flexor spasticity; however, its effects on ankle plantarflexor spasticity are uncertain.

Objective: To assess the effects of focal vibration administered by a trained operator to the ankle plantarflexor and dorsiflexor muscles on post-stroke lower limb spasticity.

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Oral mucositis is the most common oral complication of cancer patients receiving radiotherapy or chemotherapy, leading to poor quality of life. Increasing clinical studies demonstrated that thalidomide (THD) can effectively ameliorate radiation-induced oral mucositis (RIOM). Here we established an experimental mouse model, radiation-induced human oral epithelial cells (HOECs), and further investigate the underlying mechanism the THD protective effect against RIOM.

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Purpose: Laparoscopy is being increasingly accepted for pancreaticoduodenectomy. Stapled anastomosis (SA) is used extensively to facilitate laparoscopic pancreaticoduodenectomy (LPD); however, the incidence of anastomotic bleeding after stapled gastrointestinal anastomosis is still high.

Methods: One hundred and thirty-nine patients who underwent LPD using Whipple method were enrolled in our study.

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Background: This multicenter clinical trial was designed to evaluate the efficacy and safety of thalidomide (THD) in preventing oral mucositis (OM) in patients with nasopharyngeal carcinoma (NPC) undergoing concurrent chemoradiotherapy (CCRT).

Methods: Patients with locally advanced NPC were randomly assigned to either a THD group or a control group. All 160 patients received radical intensity-modulated radiotherapy plus cisplatin-based concurrent chemotherapy and basic oral hygiene guidance.

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Tongue squamous cell carcinoma (TSCC) is one of the deadliest cancers of the head and neck, but the role of the ferroptosis pathway in its development is still unknown. In this study we explored the pathogenetic mechanisms associated with ferroptosis in TSCC. We identified differentially expressed genes (DEGs) of TSCC patients and used gene ontology (GO), the Kyoto Encyclopedia of Genes and Genomes (KEGG), and gene set enrichment analysis (GSEA) to annotate, visualize, and integrate these DEGs.

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The integrity of the endothelial barrier is required to maintain vascular homeostasis and fluid balance between the circulatory system and surrounding tissues and to prevent the development of vascular disease. However, the origin of the newly developed endothelial cells is still controversial. Stem and progenitor cells have the potential to differentiate into endothelial cell lines and stimulate vascular regeneration in a paracrine/autocrine fashion.

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Overexpression of the membrane protein SEC61 translocon gamma subunit (SEC61G) has been observed in a variety of cancers; however, its role in head and neck squamous cell carcinomas (HNSCC) is unknown. This study aimed to elucidate the relationship between and HNSCC based on data from The Cancer Genome Atlas (TCGA) database. Data for HNSCC patients were collected from TCGA and the expression level of was compared between paired HNSCC and normal tissues using the Wilcoxon rank-sum test.

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Background And Aims: Characterized by hepatocyte steatosis, inflammation, and fibrosis, NASH is a complicated process that contributes to end-stage liver disease and, eventually, HCC. TNF-α-induced protein 8-like 1 (TIPE1), a new member of the TNF-α-induced protein 8 family, has been explored in immunology and oncology research; but little is known about its role in metabolic diseases.

Approach And Results: Here, we show that hepatocyte-specific deletion of TIPE1 exacerbated diet-induced hepatic steatosis, inflammation, and fibrosis as well as systemic metabolic disorders during NASH pathogenesis.

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Since the discovery of vascular stem cells, there has been considerable advancement in comprehending the nature and functions of these cells. Due to their differentiation potential to repair endothelial cells and to participate in lesion formation during vascular remodeling, it is crucial to elucidate vascular stem cell behaviors and the mechanisms underlying this process, which could provide new chances for the design of clinical therapeutic application of stem cells. Over the past decades, major progress has been made on progenitor/vascular stem cells in the field of cardiovascular research.

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Aims: microRNA-124(miR-124) has recently been reported to be elevated in cardiovascular disease. In this study, we aimed to investigate the exact role of miR-124 in cardiomyocytes and myocardial infarction, identifying the functional target and its regulatory mechanisms.

Methods And Results: Cultured cardiomyocytes, myocardial-infarction mouse model, and clinical data were used to study the effects of miR-124 on myocardial ischemia.

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PKA signaling is important for the post-translational modification of proteins, especially those in cardiomyocytes involved in cardiac excitation-contraction coupling. PKA activity is spatially and temporally regulated through compartmentalization by protein kinase A anchoring proteins. Cypher/ZASP, a member of PDZ-LIM domain protein family, is a cytoskeletal protein that forms multiprotein complexes at sarcomeric Z-lines.

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