Background: Nonalcoholic fatty liver disease (NAFLD)-including cirrhosis has emerged as a central component of the global chronic liver disease burden. Its progression is closely linked to metabolic syndrome and exhibits significant geographic and population-specific heterogeneity. This study systematically analyzed the prevalence, incidence, mortality, and disability-adjusted life years (DALYs) of NAFLD-including cirrhosis at global, regional, and national levels from 1990 to 2021, using data from the Global Burden of Disease Study 2021 (GBD 2021). Materials and Methods: Data were sourced from GBD 2021. To quantify temporal trends in age-standardized prevalence rate (ASPR), age-standardized incidence rate (ASIR), age-standardized mortality rate (ASMR), and age-standardized DALYs rate (ASDR) for NAFLD-including cirrhosis, estimated annual percentage changes were calculated for 1990–2021. Analyses were stratified by sex, 20 age-groups, 5 socio-demographic index (SDI) quintiles, 21 GBD regions and 204 countries and territories. Statistical analyses and visualizations were performed using R software (version 4.5.1). Results: In 2021, the global burden of NAFLD-including cirrhosis remained substantial. Total cases reached 1 267 815 566 (95% uncertainty interval [UI]: 1 157 880 130–1 380 382 443), with ASPR at 15 017.5 per 100 000 (13 755.8–16 360.8), ASIR at 592.8 per 100 000 (542.2–643.2), ASMR at 1.14 per 100 000 (0.82–1.52), and ASDR at 30.9 per 100 000 (22.2–41.5). Significant regional heterogeneity was observed. Low–middle SDI regions had the highest ASMR and ASDR, while middle SDI regions led in ASPR and ASIR. Geographically, Andean Latin America had the highest ASMR and ASDR globally, whereas East Asia had the lowest; North Africa and the Middle East ranked highest for ASIR and ASPR, high-income North America had the lowest ASIR, and Southeast Asia the lowest ASPR. Conclusions: Global NAFLD-including cirrhosis burden exhibits marked regional heterogeneity. High mortality in low–middle SDI regions likely reflects limited healthcare resources, while high prevalence in middle SDI regions correlates with metabolic syndrome prevalence. The extreme burden in Andean Latin America underscores the impact of restricted healthcare access. Given these findings, intervention strategies should be tailored to regional contexts. We therefore recommend prioritizing integrated metabolic management in middle SDI regions with a high burden of metabolic syndrome, and strengthening capacity for complication prevention in resource-constrained low–middle SDI regions, to effectively reduce disparities in disease burden.

BACKGROUND:Chronic pancreatitis (CP) is defined by ongoing inflammation and scarring within the pancreas, leading to loss of pancreatic function. Activation of pancreatic stellate cells (PSCs) plays a central regulatory role in acinar-to-ductal metaplasia (ADM), but the specific mechanisms behind it are not well understood. This study aims to explore the impact of PSCs on pancreatic regeneration through exosome-mediated lncRNA MALAT1 in ADM. METHODS:We established a stable cell line overexpressing Gli1 and an in vitro co-culture model with PSCs; extracted PSC exosomes for biological analysis; identified differentially expressed lncRNA-MALAT1 using lncRNA chips; and explored the functional and mechanistic changes following exosome entry into cells using molecular biology methods, confirming its regulatory effect on downstream RBPJ using dual-luciferase and FISH. Finally, we validated our findings in animal models and human specimens. RESULTS:Our results showed that overexpression of Gli1 in PSCs significantly increased their activation and upregulated markers related to pancreatic fibrosis. The differentially expressed lncRNA MALAT1 in exosomes suppressed ADM by binding RBPJ. Conversely, downregulating MALAT1 significantly promoted ADM, thereby protecting pancreatic function. CONCLUSION:After PSCs overexpress Gli1, they regulate the expression of RBPJ through lncRNA MALAT1 in exosomes to inhibit ADM pathology, thus inhibiting pancreatic regeneration, providing new insights underlying the molecular mechanisms of pancreatic regeneration in chronic pancreatitis.

Liver fibrosis is characterized by the activation and transformation of hepatic stellate cells (HSCs) induced by various injury factors. The degree of liver fibrosis can be significantly improved, but persistent injury factors present a significant therapeutic challenge. Hepatocytes are the most important parenchymal cell type in the liver. In this study, we explored the molecular mechanisms by which damaged liver cells activate HSCs through extracellular vesicles. We established a coculture model of LO2 and LX2 and validated its exosomal transmission activity. Subsequently, differentially expressed long noncoding RNAs (lncRNAs) were screened through RNA sequencing and their mechanisms of action as competing endogenous RNAs (ceRNAs) further confirmed using biological methods, such as FISH and luciferase assays. Damaged liver cells induced activation of LX2 and upregulation of liver fibrosis-related markers. Exosomes extracted and identified from the supernatant fraction contained differentially expressed lncRNA cytoskeleton regulator RNA (CYTOR) that competed with microRNA-125 (miR-125) for binding to glial cell line-derived neurotrophic factor (GDNF) in HSCs, in turn, promoting LX2 activation. MiR-125 could target and regulate both CYTOR and GDNF and vice versa, as verified using the luciferase assay. In an in vivo model, damaged liver extracellular vesicles induced the formation of liver fibrosis. Notably, downregulation of CYTOR within extracellular vesicles effectively inhibited liver fibrosis. The lncRNA CYTOR in exosomes of damaged liver cells is upregulated and modulates the expression of downstream GDNF through activity as a ceRNA, providing an effective mechanism for activation of HSCs.

Inflammatory bowel disease (IBD) is a chronic and destructive autoimmune disease that has created a global burden. However, the pathogenesis and treatment strategies of IBD remain difficult problems to overcome. The anti-inflammatory action of anion-dependent layered double hydroxide (LDH) is evaluated in IBD. Raw264.7 macrophages induced by Lipopolysaccharide (LPS) produced low levels of pro-inflammatory cytokines after LDH treatment. The results from dextran sulfate sodium (DSS)-induced murine colitis models show that LDHs significantly reduce pro-inflammatory cytokines in the colon tissue and inhibit colon atrophy. Most importantly, LDH with NO3- as the interlayer anion (LDH-NO3-) demonstrates superior anti-inflammatory ability compared to LDH with Cl- as the interlayer anion (LDH-Cl-), both in vitro and in vivo. LDH-NO3- promotes the differentiation of CD206(+)CX3CR1(+) lamina propria macrophages, reduces the abundance of T helper 17 (Th17) cells, and inhibits the activation of the IL-17 signaling pathway. LDH-NO3- also limits the pro-inflammatory effects of IL-17A on macrophages, and the anti-inflammatory effects of LDH-NO3- are reversed by IL-17RA-siRNA. Suggesting that LDH effectively inhibits the inflammatory reaction induced by the interaction between macrophages and Th17 cells. This study demonstrates that LDH-NO3- is a drug-free nanomedicine that acts against IBD, providing application prospects for LDH-NO3- in IBD treatment.

BACKGROUND:Hedgehog-Gli1 signaling induces development of two common neurological features seen in pancreatic ductal adenocarcinoma (PDAC): peripheral neural invasion (PNI) and peripheral neural remodeling (PNR). However, the underlying molecular mechanisms in cancer cells and nerves within Gli1-derived PNR have not previously been comprehensively analyzed.METHODS:In this study, RNA sequencing was used to screen meaningful circRNAs in PNR. An in vitro model of PNR was subsequently constructed through a co-culture system comprising PDAC cells and murine dorsal root ganglia (DRG) (as the neuronal element), and the relevant mechanisms were explored using a series of molecular biology experiments. A subcutaneous nude mouse tumorigenesis model was established to further verify the occurrence of PNR that was detected in human PDAC samples.RESULTS:We first confirmed the molecular mechanisms of PNR development through crosstalk between exosomal circ-0011536 and DRG. In Gli1-overpressed PDAC, circ-0011536 is mainly secreted by exosomes. After being ingested by DRG, it can promote the activity of DRG by degrading miR-451a and upregulating the expression of VGF. Overexpression of Gli1 can accelerate the proliferation of subcutaneous tumors in mice and is closely related to the density of nerve plexuses, while downregulating circ-RNA inhibits tumor proliferation and reduces the density of nerve plexuses. In addition, TMA results confirmed that Gli1 overexpression significantly increased the expression of VGF and was closely associated with increased nerve plexus density.CONCLUSION:Hedgehog-Gli1-induced exosomal circ-0011536 promoted PNR via the miR-451a/VGF axis, thereby establishing that it may contribute to PDAC-associated nerve changes with activated Hedgehog signaling.

Aim Acute lung injury (ALI) is a common complication of severe acute pancreatitis (SAP) with a high mortality. Early prediction of patients at risk in initial stage can improve the long-term survival. Methods A total of 91 patients with SAP out of 1647 acute pancreatitis patients from January 2015 to December 2020 were considered. A predictive model for SAP-associated ALI was constructed based on the valuable risk factors identified from routine clinical characteristics and plasma biomarkers. The value of the model was evaluated and compared with Lung Injury Prediction Score (LIPS). A nomogram was built to visualize the model. Results Diabetes, oxygen supplementation, neutrophil count and D-dimer were found to be associated with ALI in SAP. The predictive model based on these factors had an area under the receiver operating characteristic curve [AUC: 0.88, 95% confidence interval (CI): 0.81–0.95], which was superior to LIPS (AUC: 0.71, 95% CI: 0.60–0.83), also with the higher sensitivity (65%) and specificity (96%) than LIPS (62%, 74%, respectively). Decision curve analysis of the model showed a higher net benefit than LIPS. Visualization by a nomogram facilitated the application of the model. Conclusion Diabetes, oxygen supplementation, neutrophil count and D-dimer were risk factors for SAP-associated ALI. The combination of these routine clinical data and the model visualization by a nomogram provided a simple and effective way in predicting ALI in the early phase of SAP.

Continuous assessment of disease activity remains a huge challenge during the follow-ups of patients with Crohn’s disease (CD). In this paper, we aimed to evaluate the performance of contrast-enhanced ultrasound (CEUS) by comparing with computed tomography enterography (CTE) in the assessment of disease activity in CD. Fifty-two patients diagnosed with CD were included in this study, using the CEUS and CTE as imaging methods for comparison. The selected parameters included the location and thickness of the thickest part of the intestinal wall, mesenteric fat proliferation, mesenteric vessels change, enhancement pattern and the presence of complications. Patients were clinically assessed using the Crohn's disease activity index (CDAI), C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Simple endoscopic score for Crohn’s disease (SES-CD) was regarded as the reference standard. The location of the thickest part of the intestinal wall (κ = 0.653), bowel wall thickness (ICC = 0.795), mesenteric vessels change (κ = 0.692) and complications (κ = 0.796) displayed substantial agreement (0.61–0.80) between CEUS and CTE, while the detection of mesenteric fat proliferation (κ = 0.395) and enhancement pattern (κ = 0.288) showed fair consistency (0.21–0.40) for comparison. In CEUS, bowel wall thickness, mesenteric fat proliferation, enhancement pattern and mesenteric vessels change were statistically significant in assessing CD activity, while bowel wall thickness, mesenteric fat proliferation and mesenteric vessels change in CTE. Bowel wall thickness showed the best diagnostic performance in the assessment of CD activity at CEUS and CTE. CEUS provides a radiation-free and effective way to assess the CD activity in comparison with CTE, which also avoids frequent colonoscopy examinations, improves tolerance of patients, and reduces the cost of medical care, thereby serving as a useful tool for CD follow-up.

The discovery of a potent photosensitizer with desirable immunogenic cell death (ICD) ability can prominently enhance antitumor immunity in photodynamic therapy (PDT). However, majority of commercially-available photosensitizers suffer from serious aggregation and fail to elicit sufficient ICD. Pyroptosis as a newly identified pattern for potent ICD generation is rarely disclosed in reported photosensitizers. In addition, the photosensitizer with excellent mitochondria-anchored ability evokes prominent mitochondria oxidative stress, and consequently induces ICD. Herein, a novel supramolecular photosensitizer LDH@ZnPc is reported, without complicated preparation, but reveals desirable pyroptosis-triggered ability with mitochondria anchoring feature. LDH@ZnPc is obtained through isolation of ZnPc using positive charged layered double hydroxides (LDH), and excellent mitochondria-anchored ability is achieved. More importantly, LDH@ZnPc-mediated PDT can effectively initiate gasdermin D (GSDMD)-dependent pyroptosis of tumor cells. In vitro and in vivo results verify robust ICD ability and potent tumor inhibition efficacy, and antitumor immunity towards distant tumor inhibition. This study reveals that LDH@ZnPc can act as an excellent pyroptosis inducer with simultaneous mitochondria anchoring ability for enhancing photodynamic therapy and boosting antitumor immunity.

Background and aims Endoscopic submucosal dissection (ESD) is an advanced minimally invasive technique for en bloc resection of superficial gastrointestinal lesions, which is drawn an increasing attention from its emergence. This bibliometric analysis is to evaluate the origin, current hotspots, and research trends on ESD. Methods A total of 2,131 publications on ESD from 2006 to 2020 were obtained from the Web of Science Core Collection (WoSCC) database. Bibliometric visualization analyses of countries/regions, institutes, authors, journals, references and keywords were performed by CiteSpace V.5.8.R3. Results The quantity of publications on ESD increased significantly during the past 15 years. Japan occupied the leading position in terms of research power. Professor Yutaka Saito, together with the institute he belongs, the Endoscopy Division, National Cancer Center Hospital, Tokyo, Japan, were the most productive author and institute, respectively. Colorectal ESD led the main thematic concentrations in ESD research. The most prolific journal was Gastrointestinal Endoscopy. European ESD Guideline was the most frequently co-cited reference. Guideline, meta-analysis, endoscopic resection, poly-glycolic acid sheet, Barrett's esophagus, fibrin glue, risk and colorectal neoplasm will be the active research hotspots in the future. Conclusions These findings provide the trends and frontiers in the field of ESD, as well as valuable information for clinicians and scientists to discover the future perspectives with potential collaborators.

目的 评估内镜下特征联合Ki67判断早期结直肠癌(early colorectal cancer,ECC)黏膜下浸润深度的准确性.方法 收集2019年09月—2022年01月上海第十人民医院内镜中心接受内镜治疗并经术后病理诊断为非浸润性高级别瘤变(high-grade neoplasia,HGN)、黏膜内癌(intramucosal carcinoma,MC)和黏膜下浸润癌(submucosal invasive carcinoma,SMIC)的132例患者的临床病理资料,通过分析ECC的白光内镜下特征、基于NBI内镜下的JNET分型、免疫组化方法检测到Ki67的表达,探讨内镜下特征联合病理免疫组化判断ECC浸润深度的准确性.结果 MC组病灶直径>30 mm占比最高(P<0.05),SMIC组病灶表面存在中央凹陷的占比显著高于HGN组、MC组(P<0.05).有序多因素Logistic回归分析显示:位于左半结肠及直肠、表面存在中央凹陷、黏膜颜色较周围正常黏膜颜色红和Ki67阳性细胞比率>25％是结直肠病灶发生黏膜下浸润的独立危险因素.ROC曲线分析显示JNET分型联合Ki67阳性细胞比率评估黏膜下深层浸润具有非常高诊断价值(AUC=0.952,95％CI:88.32％～102.16％).结论 本组ECC在白光内镜下的特征难以准确判断SMIC的浸润深度,而JNET分型联合Ki67阳性细胞比率可提高评估黏膜下浸润深度的准确性.

The mucosa microenvironment is critical for intestinal stem cell self-renewal and reconstruction of the epithelial barrier in inflammatory bowel disease (IBD), where the mechanisms underlying cross-talk between intestinal crypts and the microenvironment remain unclear. Here, we firstly identified miR-494-3p as an important protector in colitis. miR-494-3p levels were decreased and negatively correlated with the severity in human IBD samples, as well as in colitis mice. In colitis crypts, a notable cytokine–cytokine receptor, miR-494-3p-targeted EDA2R and the ligand EDA-A2, suppressed colonic stemness and epithelial repair by inhibiting β-catenin/c-Myc. In differentiated IECs, miR-494-3p inhibits macrophage recruitment, M1 activation and EDA-A2 secretion by targeting IKKβ/NF-κB in colitis. A miR-494-3p agomir system notably ameliorated the severity of colonic colitis in vivo. Collectively, our findings uncover a miR-494-3p-mediated cross-talk mechanism by which macrophage-induced intestinal stem cell impairment aggravates intestinal inflammation.

联动成像(linked color imaging,LCI)内镜以增强病灶与周围黏膜的颜色对比度为主要特点,在多种消化道疾病的筛查、诊断上显现出特有的优势.胃癌是我国最常见的恶性肿瘤之一,早期诊断能减少外科手术率、明显改善患者预后.但目前早期胃癌(early gastric cancer,EGC)的诊断率较低,使用普通白光内镜容易漏诊.LCI作为新型的图像增强内镜,已被众多研究证实能够有效提高EGC的诊断率,并有助于EGC与炎症、肠上皮化生的鉴别诊断.此外,在幽门螺杆菌根除后胃癌的筛查与风险评估方面,LCI也具有一定的优势.将LCI与其他内镜技术联用可进一步提升诊断EGC的准确率.因此,LCI在EGC的诊断上具有很好的应用前景.本文将对LCI在EGC诊断方面的研究进展进行阐述,探讨现有研究的不足,以期为今后的进一步完善和探索提供一些有益的参考.

Objectives: The aim of this study was to develop an ultrasound consolidated score (UCS) in determining the activity of Crohn’s disease (CD) and evaluate it with reference to simple endoscopic score (SES). Methods: From June 2014 to June 2017, 66 patients with CD were retrospectively enrolled in this study. Each patient underwent endoscopy and transabdominal ultrasound (US) examination. The morphological symmetry, echogenicity of bowel wall, bowel wall layer structure, echogenicity of peri-bowel fat, bowel wall thickness (BWT), and Limberg type on power Doppler US were assessed with transabdominal US, and an UCS scoring system was developed based on these characteristics. Endoscopic results were used as the reference standard and SES was calculated to determine the CD activity. Receiver operating characteristic curve analysis was performed to assess the diagnostic performance for determining CD activity and the correlation between UCS and SES was assessed using Spearman correlation analysis. Results: 330 intestinal segments in 66 patients were included. The UCS of the segments in the remission phase ranged from 3.0 to 9.0 (mean, 3.6 ± 0.9) whereas in the active phase from 3.0 to 20.0 (mean, 10.6 ± 4.0) (p < 0.001). The cut-off value of UCS was 6. The associated area under ROC curve, sensitivity, specificity, positive predictive value, negative predictive value, and accuracy were 0.980, 88.3%, 95.5%, 93.8%, 91.3%, and 92.3%, respectively. The correlation coefficient between UCS and SES was 0.90, which was higher than the correlation coefficient of 0.83 between BWT and SES. Conclusions: The newly developed UCS with transabdominal US has a good performance and potentially provides an effective alternative for evaluating the activity of CD. Advances in knowledge: UCS is an effective method to evaluate the activity of CD because it provides comprehensive information of the disease. Therefore, it could be employed as an alternative for diagnosis of CD.

Objectives The aim of this study was to evaluate the diagnostic performance of strain elastography, acoustic radiation force impulse (ARFI) imaging and point shear wave elastography (p‐SWE) for assessment of the predominant types of intestinal stenosis in Crohn disease. Methods Twenty‐five patients were enrolled in this study, among whom 25 suspicious stenoses in 25 intestinal segments were studied using gray scale ultrasonography. All 3 elastography methods were performed, and all patients underwent endoscopy within 24 hours with pathologic biopsy. The sensitivity, specificity, accuracy, positive predictive value (PPV), negative predictive value (NPV), Youden index, and area under the receiver operating characteristic curve (AUROC) were calculated. Pathologic findings were regarded as the gold standard. Results For SE, the optimal cutoff value was a score of 4 or greater (sensitivity, 75%; specificity, 66.7%; accuracy, 68%; PPV, 30%; NPV, 93.3%; AUROC, 0.708; however, P > .05). The results of ARFI imaging were similar: the optimal cutoff value was a score of 4 or greater (sensitivity, 50%; specificity, 81%; accuracy, 76%; PPV, 33.3%; NPV, 89.4%; AUROC, 0.669; P < .05). However, for p‐SWE, the optimal cutoff value was reached when the shear wave velocity exceeded 2.73 m/s (sensitivity, 75%; specificity, 100%; accuracy, 96%; PPV, 100%; NPV, 95.5%; AUROC, 0.833; P < .05). Conclusions p‐SWE had the best performance for evaluating and differentiating intestinal stenosis in Crohn disease, while neither SE nor ARFI imaging achieved satisfactory outcomes for evaluating inflammatory stenosis and fibrotic stenosis of Crohn disease.

Metastasis to distant organs is a particularly ominous feature of malignant cancer. LKB1 (also known as STK11) has been identified as a tumor suppressor in several types of cancers. Here, we show that LKB1 is at low levels and is negatively associated with poor clinical outcomes in pancreatic cancer (PC). LKB1 is inversely correlated with Snail protein in PC, in which the loss of LKB1 facilitates metastasis through elevating Snail protein level. Furthermore, LKB1 boosts Snail's interaction with E3 ligase FBXL14, leading to increasing ubiquitin-mediated Snail degradation. Notably, metformin could increase Snail protein ubiquitination via augmenting the location of LKB1 at cytoplasm as well as increasing LKB1 expression. Altogether, our data established that LKB1 impedes invasion and metastasis by decreasing the Snail protein level in PC. Targeting the LKB1/FBXL14/Snail axis may represent a promising therapeutic strategy and metformin might be beneficial for PC therapy through activating the LKB1-mediated Snail ubiquitination pathway.

Severe acute pancreatitis is a disease involving multiple organs and systems and can lead to a series of complications .It is reported that a quarter of patients with severe pancreatitis may develop vascular complications , which is the major cause of death.Vascular complications can be divided into intravenous and arterial complications .Diagnosis and treatment should be given according to clinical manifesta - tions, laboratory results, and imaging findings, and at present, individualized treatment is emphasized in clinical diagnosis and treatment .This article reviews the advances in the diagnosis and treatment of vascular complications of acute pancreatitis .

Previous studies have focused on the effects of propylene glycol alginate sodium sulfate (PSS) against thrombosis, but the anti‐inflammatory potential is unknown. Therefore, we specifically focused on the protective effects of PSS on cerulein‐induced acute pancreatitis (AP) using a mouse model, and investigated the mechanism of PSS on autophagy and apoptosis via the Mitogen‐activated protein kinase (MEK)/extracellular signal‐regulated kinase (ERK) pathway. Cerulein (100 ug/kg) was used to induce AP by ten intraperitoneal injections at hourly intervals in Balb/C mice. Pretreatment with vehicle or PSS was carried out 1 h before the first cerulein injection and two doses (25 mg/kg and 50 mg/kg) of PSS were injected intraperitoneally. The severity of AP was assessed by pathological score, biochemistry, pro‐inflammatory cytokine levels, myeloperoxidase (MPO) activity and MEK/ERK activity. Furthermore, pancreatic histological scores, serum amylase and lipase activities, tumor necrosis factor‐α (TNF‐α), interleukin (IL)‐1β interleukin (IL)‐6 levels, and MPO activity were significantly reduced by PSS via up‐regulated MEK/ERK activity. The representative molecules of apoptosis and autophagy, such as Bcl‐2, Bax, Lc‐3, Beclin‐1, P62, were remarkably reduced. Taken together, these results indicate that PSS attenuates pancreas injury by inhibiting autophagy and apoptosis through a mechanism involving the MEK/ERK signaling pathway.

Objectives Seasonal variation on acute pancreatitis (AP) has not been investigated in Eastern Asia. The aims of the study were to assess the association of the onset of AP with the occurrence of seasons and Chinese festivals and to investigate trends in AP incidence in Shanghai, China. Methods From January 2009 to December 2014, a total of 1780 patients with AP were considered. The incidence was assessed by different etiology and severity. Monthly disease prevalence was investigated to explore the seasonal variation. The prevalence on weekdays, weekends, and festivals was evaluated to establish any weekly or festival influences in AP. Results Acute pancreatitis increased from 30.5 per 100,000 in 2009 to 39.2 in 2014 (5.1% annual increase), with greatest increases in alcoholic (19.8% annually) and severe AP (13.7% annually). Time series analysis indicated that prevalence was significantly higher form February to May (spring) and from September to October (autumn). Acute pancreatitis increased during Chinese festivals, 17% and 28% greater than that observed on weekdays and weekends, respectively. Prevalence was greatest in Chinese Spring Festival week. Conclusions Acute pancreatitis increased in Shanghai and had a seasonal variation, with a higher frequency of events in the spring and autumn. Chinese festivals are associated with a high prevalence of AP.

Chronic pancreatitis is a progressive chronic inflammatory disease and finally progresses to irreversible pancreatic fibrosis.The diagnosis and treatment of chronic pancreatitis is difficult and there are still no effective measures for delaying or reversing fibrosis.This article introduces the research advances in the role of microRNA (miRNA) in the fibrosis of chronic pancreatitis and points out that pancreatic stellate cell activation is the key step in pancreatic fibrosis.Recent studies have demonstrated that miRNA regulates pancreatic stellate cell activation and participates in the fibrosis of chronic pancreatitis through altering gene expression and mediating signaling pathways and epithelial -mesenchymal transition,and miRNA may become a new target for the treatment of chronic pancreatitis.