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Furthermore, the proangiogenic activity of MMP2 is one of the potential mechanisms that are associated with both pathological situations. In the present article, the latest research on MMP2 in bone homeostasis is reviewed and the mechanisms underlying the role of this protein in skeletal metastasis and developmental osteolysis are discussed.Inonotus obliquus (IO) is an edible fungus that exerts various biological functions, including anti‑inflammatory, antitumor and immunomodulatory effects. The present study was designed to investigate the role of IO extract (IOE) in myocardial ischemia/reperfusion (MI/R) and determine the exact molecular mechanisms. The left anterior descending coronary artery was ligated to establish the MI/R injury model in rats. IOE exhibited a novel cardioprotective effect, as shown by improvement in cardiac function and decrease in infarct size. Pretreatment with IOE activated antioxidant enzymes in cardiomyocytes, including glutathione peroxidase, superoxide dismutase and catalase. PRT543 IOE pretreatment also induced the upregulation of NAD‑dependent protein deacetylase sirtuin‑1 (SIRT1) and downregulation of glucose‑regulated protein 78, phosphorylated (p‑) protein kinase R‑like endoplasmic reticulum kinase, p‑eukaryotic translation initiation factor 2 subunit α, C/EBP homologous protein and caspase‑12. Furthermore, IOE alleviated endoplasmic reticulum (ER) stress‑induced apoptosis in cardiomyocytes by decreasing the mRNA levels of caspase‑12. IOE inhibited apoptosis induced by overexpression of pro‑caspase‑9 and pro‑caspase‑3. In summary, IOE pretreatment protects the heart against MI/R injury through attenuating oxidative damage and suppressing ER stress‑induced apoptosis, which may be primarily due to SIRT1 activation.Although long non‑coding RNAs (lncRNAs) have been implicated in various human cancer types, the role of lncRNA ezrin antisense RNA 1 (EZR‑AS1) in cutaneous squamous cell carcinoma (cSCC) remains unclear. The present study aimed to investigate the effect of lncRNAEZR‑AS1 on cSCC and identify the underlying molecular mechanisms. EZR‑AS1 expression was measured in cSCC tissue and cells detected using reverse transcription‑quantitative PCR. Gain‑of‑function assays were performed in A431 cells, which have a relatively low expression of EZR‑AS1, while loss‑of‑function assays were performed in SCC13 and SCL‑1 colon cancer cells, which have a relatively high expression of EZR‑AS1. Cell viability, proliferation, migration, invasion and apoptosis were assessed using MTT, plate cloning, wound healing, Transwell and flow cytometry assays, respectively. EZR‑AS1 mRNA expression levels were significantly upregulated in cSCC tissues and cells compared with adjacent healthy tissues and HaCaT cells, respectively. Compared withg the PI3K/AKT signaling pathway. Therefore, the present study provided novel insights into the diagnosis and treatment of cSCC.Elevated intracranial pressure (ICP) is one of the most common complications following an ischemic stroke, and has implications for the clinical and neurological outcomes. The aim of the present study was to examine whether elevated ICP may increase IL‑1β and IL‑18 secretion by activating the NOD‑like receptor protein 3 (NLRP3) inflammasome in microglia of ischemic adult rats. Sprague‑Dawley rats that underwent middle cerebral artery occlusion were used for assessment of ICP. Reactive oxygen species (ROS) production was detected, and western blotting and immunofluorescence staining were used to determine the expression levels of Caspase‑1, gasdermin D‑N domains (GSDMD‑N), IL‑1β and IL‑18 in microglial cells. ICP levels were significantly increased, which was accompanied by ROS overproduction, in the brain tissue following ischemia‑reperfusion (IR) injury in rats. Treatment with 10% hypertonic saline by intravenous injection significantly reduced the ICP and ROS levels of the rats. Furthermore, high pressure (20 mmHg) combined with oxygen‑glucose deprivation (OGD) treatment resulted in increased ROS production in BV‑2 microglial cells compared with those subjected to OGD treatment alone in vitro. Elevated pressure upregulated the expression of Caspase‑1, GSDMD‑N, IL‑18 and IL‑1β in IR‑treated or OGD‑treated microglia both in vivo and in vitro. More importantly, Caspase‑1, GSDMD‑N, IL‑18 and IL‑1β expression in microglia was significantly downregulated when elevated pressure was reduced or removed. These results suggested that elevated ICP‑induced IL‑1β and IL‑18 overproduction via activation of the NLRP3 inflammasome by ischemia‑activated microglia may augment neuroinflammation.Cisplatin (DDP) resistance is a major obstacle in the chemotherapeutic efficacy of ovarian cancer. The present study aimed to explore the role of miR‑576‑3p in DDP sensitivity of ovarian cancer cells. Ovarian cancer cell lines SKOV3 and A2780 and DDP‑resistant ovarian cancer cell lines SKOV3/DDP and A2780/DDP were used in the present study. In vitro studies demonstrated that microRNA (miR)‑576‑3p overexpression increased the DDP sensitivity of DDP‑resistant ovarian cancer cells. A dual‑luciferase assay verified that both programmed death‑ligand 1 (PD‑L1) and cyclin D1 were targets of miR‑276‑3p and were reversely associated with the expression of miR‑576‑3p. Moreover, in vivo studies indicated that tumorigenesis was inhibited by DDP, which was enhanced by further miR‑576‑3p overexpression in tumor tissues. Taken together, the results suggested that miR‑576‑3p overexpression increased DDP chemosensitivity of ovarian cancer cells via decreasing PD‑L1 and cyclin D1, indicating that miR‑576‑3p may serve as a promising therapeutic target for ovarian cancer.Subsequently to the publication of the above article, the authors have realized that the bar charts shown for Fig. 3A and B, as they appeared in the paper, were the same as the bar charts shown for Fig. 4B and D. link2 Fig. 3, as it should have appeared, is shown below. All the authors agree to this Corrigendum. Note that the revisions made to this figure do not adversely affect the results reported in the paper, or the conclusions stated therein. The authors regret that the duplication of the histograms in Fig. 4 as Fig. 3 was not noticed prior to the publication of this article, and offer their apologies to the Editor of Molecular Medicine Reports and to the readers of the Journal. [the original article was published in Molecular Medicine Reports 22 4611-4618, 2020; DOI 10.3892/mmr.2020.11564].Sepsis‑induced blood vessel dysfunction is mainly caused by microvascular endothelial cell injury. However, the mechanism underlying sepsis‑induced endothelial cell injury remains unclear. The present study hypothesized that sepsis‑induced inflammatory injury of endothelial cells may be the first step of endothelial barrier dysfunction. Therefore, the present study aimed to uncover the mechanism underlying the inflammatory effects of sepsis. A rat model of cecal ligation and puncture‑induced sepsis was established, and septic serum was collected. link3 Subsequently, human umbilical vein endothelial cells (HUVECs) were treated with the isolated septic or normal serum. HUVEC viability was assessed using a Cell Count Kit‑8 assay. Furthermore, transmission electron microscopy and reverse transcription‑quantitative PCR (RT‑qPCR) analysis were carried out to observe the cell morphology and determine the mRNA expression levels in septic serum‑induced HUVECs. The protein expression levels were evaluated by western blot ana‑acetylcysteine, the ERK1/2 inhibitor PD98059, the p38 inhibitor SB203580, the JNK inhibitor SP610025 or the NF‑κB inhibitor pyrrolidine dithiocarbamate restored the septic serum‑induced IL‑1β, IL‑6 and TNF‑α expression. In conclusion, the results of the current study suggested that the septic serum‑induced endothelial cell injury may be mediated by increasing ROS generation, activation of mitogen‑activated protein kinases and NF‑κB translocation.Transforming growth factor β1 (TGF‑β1) is one of the most important fibrogenic factors promoting the activation of hepatic stellate cells (HSCs). Autophagy is a process used by cells to degrade and recycle cellular proteins. Although TGF‑β1 induces autophagy in several other cellular systems, the association between its effect on fibrogenesis and autophagy in HSCs have not been determined. Liver tissues from C57BL/6 mice and the mouse HSC line JS1 were analyzed. Acute and chronic liver injury models were induced by carbon tetrachloride (CCl4), and JS1 cells were stimulated by TGF‑β1 to assess the mechanism and relationship between autophagy and fibrosis. Liver tissues from acute and chronic injury models induced by CCl4 demonstrated evidence of increased autophagic activity, as assessed by the expression of the microtubule‑associated protein 1 light chain 3BII protein. TGF‑β1 stimulated the activation of JS1 cells and simultaneously increased autophagy flux. However, this effect was attenuated when autophagy was inhibited using chloroquine, 3‑methyladenine or lentiviral short hairpin RNA‑mediated knockdown of autophagy‑related gene 7. Furthermore, whether MAPK, including ERK, JNK and p38 MAPK cascades were associated with TGF‑β1‑induced autophagy in JS1 cells was determined. Subsequently, it was shown that the ERK inhibitor, PD98059, and JNK inhibitor, SP600125, were able to reverse TGF‑β1‑induced autophagy and fibrosis. The results of the present study suggest that TGF‑β1‑induced autophagy is involved in the activation of JS1 cells, possibly through activation of the ERK and JNK signaling pathways.Preeclampsia (PE) is a pregnancy‑specific complication characterized by hypertension and proteinuria, and it is one of the primary global causes of maternal and perinatal mortality. Poor remodeling of placental arteries and endothelial dysfunction serve important roles in the pathogenesis of PE. Peptide derived from complement C4 A chain (PDCC4) was identified in our previous peptidome analysis of serum from patients with PE. The present study aimed to investigate the effect of PDCC4 on endothelial dysfunction in PE. TNF‑α stimulated HUVECs were employed to mimic endothelial dysfunction in PE, and Cell Counting Kit 8 assay, wound healing assay, tube formation assay, RNA‑sequencing (seq) and western blot analysis were performed using HUVECs. Moreover, an in vivo model of PE was established using pregnant rats treated with lipopolysaccharide (LPS), and blood pressure monitoring, histopathological examination, ELISA and immunohistochemistry were performed on rats. It was found that TNF‑α impaired proliferation, migration and tube formation of HUVECs, but pretreatment with PDCC4 moderated these effects. RNA‑seq and western blotting demonstrated that the PI3K/mTOR/HIF1α signaling pathway was activated by PDCC4, and a selective PI3K inhibitor reversed the protective function of PDCC4 on TNF‑α stimulated HUVECs. Additionally, PDCC4 alleviated hypertension, histopathological changes of placenta and kidney and the expression levels of endothelial injury markers and inflammatory cytokines induced by LPS in rats. These results suggested that PDCC4 relieved endothelial dysfunction in PE via PI3K/mTOR/HIF1α signaling pathway and may be a potential therapy for PE.