Jinge Kong's research while affiliated with Peking University and other places

... Annexin A1 (ANXA1 18 ) is a glucocorticoid-regulated protein 19 that has anti-inflammatory and pro-resolving functions. 20,21 This 37 kDa protein is expressed in a wide variety of cells including cardiomyocytes, cardiac fibroblasts 20 and endocardial cells of the heart, 22 epithelial cells of the lungs, 20 mesangial and epithelial cells of the kidney, 20 endothelial cells, 23 vascular smooth muscle cells, 24 fibroblast cells, 25 liver macrophages, 26 T and B cells, neutrophils, monocytes, mast cells, and macrophages. 20 ANXA1 causes its pro-resolving effects by binding to the G-protein-coupled receptors (GPCRs) formyl peptide receptor (FPR) 1 and 2. [27][28][29] ANXA1 deficiency increases neutrophil migration and the expression of pro-inflammatory cytokines, exacerbating inflammatory responses in several disease models, including diabetes, 30 arthritis, 31,32 ulcerative colitis, 33 systemic lupus erythematosus, 34 and atherosclerosis, 35 suggesting that the proresolving mediator ANXA1 plays an important protective role in many chronic inflammatory conditions. ...

... Studies have shown that treatment with sorafenib inhibits the viability, invasion, metastasis, and EMT of HCC cells after heat exposure. 128 In addition, Zhang et al. showed that sorafenib blocks the interaction between the ECM protein collagen I and residual HCC cells by disrupting ERK signaling, thereby preventing tumor progression. 60 However, heat-induced hypoxia enhances the tolerance of HCC cells to sorafenib. ...

... Mi RNAs namely miR-30e and miR-126 [23,24] biomarkers for predicting NR in STEMI patients Elevated HPSE and EDN-1 [25][26][27] are associated with no-reflow in STEMI • MALAT1 regulates the expression of miR-155 • Expression of MALAT1 is significantly increased and that of miR-30e, miR-126 and miR-155 suppressed in the patients with NR Expression of C-reactive protein (CRP), Heparanase (HPSE) and (Endothelin-1) EDN1 is significantly up-regulated in patients with no-reflow. [28] CRP causes microvasculature obstruction by complementary activation and neutrophil plugging and contributes to NRP. ...

... Moreover, increasing evidence suggests that coffee consumption reduces the risk of multiple cancers, such as glioblastoma [5,6], colorectal cancer [7], skin cancer [8], and liver cancer [9]. It has been reported that caffeine and its analog CGS 15943 inhibit the progression of HCC via Akt signaling pathway [10,11]. And caffeine has the function of increasing the anti-tumor effect of cisplatin on cell proliferation and apoptosis in HCC cell lines [12], which indicates that caffeine-assisted chemotherapy is useful for HCC treatment. ...

... PAF: Experiments on animal models showed that PAF plays an important role in the pathogenesis of cardiovascular disorders, and some studies performed in humans reported elevated PAF levels in patients, with increased risk of ischemic events in those with coronary artery disease [68][69][70] (see Table 2). In particular, PAFs seems to stimulate reactive oxygen and nitrogen species, thus triggering the oxidative and nitrosative stress pathways, inducing vasoconstriction [128]. ...

... 85 Degradation of collagen plays an important role in the process of tumor invasion and metastasis. Several studies have reported that the expression levels of MMP2 and MMP9 are upregulated after TA. 70,86 IRFA has been demonstrated to induce the upregulation of integrin 3 and mediate the increase in MMP2 expression by activating the FAK/PI3K/AKT pathway, thereby enhancing the metastatic ability of HCC cells. 87 HMGB1 from dead tumor cells after IRFA activates the ERK1/2 pathway by binding to the receptor for advanced glycation end product and upregulates the expression of MMP2, MMP9, and cyclin E1, ultimately promoting the proliferation and migration of residual HCC. ...

... It should be noted that one study failed to demonstrate binding of MPO-modified HDL to SR-BI [87]. MPO-modified HDL is dysfunctional in preventing an enhancement of endothelial proliferation/migration and subsequent wound healing [89][90][91] (Figure 2). an enhancement of endothelial proliferation/migration and subsequent wound healing [89][90][91] (Figure 2). ...

... Indeed, RFA appears to promote a more aggressive phenotype in residual tumor cells. In fact, RFA is thought capable of promoting pro-tumorigenic processes such as proliferation, migration, EMT, increased stemness as well as neo-angiogenesis [9,21,[24][25][26][27][28]. ...

... A key factor for these adverse effects is the response of the liver parenchyma that is included in the ablation zone. Upon exposure to hyperthermia, hepatocytes release multiple signaling molecules including extracellular heat shock proteins 8,[11][12][13][14] and upregulate a host of inflammatory cytokines including tumor necrosis factor-α (TNFα) and interleukin (IL)-6 15,16 that can drive inflammationmediated carcinogenesis and result in local and remote tumor growth 6,17 . ...

... During this process, hydrogen peroxide (H2O2) is used to induce the oxidation of CI-ions catalyzed by neutrophil-derived myeloperoxidase (MPO) [37]. Conversion of this normally very unreactive halide ion into hypohalous acids means generating strong oxidizing agents capable of exerting aggressive oxidative interactions with the functional groups of various biologically important molecules and causing tissue damage [38,39]. It is thought to be important in the progression of several diseases, including cancer -hypochlorite-induced oxidative stress has been proven to elevate the capability of highdensity lipoprotein (HDL), in promoting breast cancer metastasis [40]. ...