Abstract:Objective：This study aimed to investigate the potential of quercetin（Que）in ameliorating non-alcoholic fatty liver disease （NAFLD）induced by a high-fat diet（HFD）through the modulation of endoplasmic reticulum stress（ERS）in rats. Methods： Feeding SD rats with high-fat diet（HFD）for 8 weeks to establish the NAFLD model，then randomly divided into the HFD group，HFD + low-dose Que group（25 mg/kg），and HFD + high-dose Que group（50 mg/kg）. Another group of rats fed normal diet served as the control group. During the administration period，monitoring of rat body weight and food intake was conducted. After continuing feeding for 8 weeks，serum levels of total cholesterol（TC），triglycerides（TG），low-density lipoprotein cholesterol（LDL-C），high-density lipoprotein cholesterol（HDL-C），alanine aminotransferase（ALT），aspartate aminotransferase（AST），as well as changes in TC and TG content in liver tissue of each group were detected. Histopathological changes in rat liver tissue were observed by hematoxylin -eosin （HE）staining，oil red O staining，and Masson’s staining. Blood glucose levels were measured using a glucometer，and rat glucose tolerance was assessed by glucose tolerance test. Fasting insulin levels in each group of rats were detected using enzyme-linked immunosorbent assay（ELISA）kits. Real-time fluorescent quantitative PCR was used to detect the expression changes of ERS-related genes Bip，Atf6，Atf4，Xbp-1s，and Chop in rat liver tissue of each group. Western blot was used to detect the expression changes of ERS-related proteins BiP，CHOP，ATF4，ATF6，XBP-1s，and XBP-1u in rat liver tissue of each group. Results：Throughout the experiment， no significant differences in food intake and body weight were observed among the four groups. Compared to the control group，the HFD group exhibited increased serum levels of triglycerides（TG），total cholesterol（TC），low-density lipoprotein-cholesterol（LDL-C）， glutamic oxalacetic transaminase（AST），and glutamic-pyruvic transaminase（ALT），along with decreased high-density lipoprotein-cholesterol（HDL-C）levels（P < 0.05）. In the low-dose Que group，serum levels of TG，TC，LDL-C，AST，and ALT were significantly reduced compared to the HFD group（P < 0.05）. Similarly，the high-dose Que group showed decreased serum levels of TG，TC，AST， and ALT compared to the HFD group（P < 0.05）. In the HFD group，the liver exhibited enlargement and increased absolute weight， with prominently swollen hepatocytes，marked vacuolization，and accumulated lipid droplets. Additionally，increased collagen deposition，insulin resistance，and impaired glucose tolerance were observed in the HFD group. However，these alterations were reversed in both low-and high-dose Que groups. The results of RT-qPCR and Western blot showed that compared to the control group， the mRNA expression of Bip，Atf6，Atf4，Xbp-1s，and Chop in the liver tissue of rats in the HFD group significantly increased，and the protein expression of BiP，CHOP，ATF4，ATF6，and XBP-1s also significantly increased. Compared to the HFD group，the mRNA expression of Bip，Atf6，Atf4，Xbp-1s，and Chop in the liver tissue of rats in the low-and high-dose Que groups decreased，and the protein expression of BiP，CHOP，ATF4，ATF6，and XBP -1s also significantly decreased. Conclusion：Que treatment attenuates HFD-induced aberrant lipid metabolism，impaired glucose tolerance，and hepatic lipid deposition in NAFLD rats，with modulation of the ERS-related pathway potentially playing a critical role.

Abstract:Objective：To explore whether p53 heterozygote attenuates osteoporosis phenotype of 1，25（OH）₂D₃ deficient mice by enhancing the antioxidant capacity. Methods：The long bones of 10-week-old wild type（WT）mice，p53 heterozygote（p53^+/-）mice， 1α-hydroxylase knockout［1α（OH）ase^-/-］mice，and 1α（OH）ase^-/-p53^+/- mice，fed on a high-calcium and high-phosphorus diet，were analyzed and compared using X-ray，micro -CT，histopathological and molecular biology methods to observe and compare changes in serum levels，bone mineralization，bone formation，bone absorption，and oxidative stress expression. Results：Compared with WT mice， p53^+/- mice showed no significant differences in serum calcium，phosphorus，parathyroid hormone（PTH），and 1，25（OH）₂D₃ levels，but had the increased bone density，total collagen（T-col）positive area，osteoblast number，alkaline phosphatase（ALP），and typeⅠcollagen （col-Ⅰ）positive area，along with the decreased levels of reactive oxygen species and the increased expression of the antioxidant enzyme SOD1. Compared with 1α（OH）ase^-/- mice，1α（OH）ase^-/-p53^+/- mice showed no significant differences in serum calcium，phosphorus， and PTH levels，with undetectable levels of 1，25（OH）₂D₃ in the serum，but showed significantly increased bone density，Tcol positive area，osteoblast number，ALP and Col-Ⅰ positive area，decreased osteoclast number and reactive oxygen species levels，and increased expression of SOD1. Conclusion：Half-dose deletion of p53 can attenuate osteoporosis phenotype of 1，25（OH）₂D₃ deficient mice by enhancing the antioxidant capacity.

Abstract:Objective：To elucidate the physiological functions of coenzyme Q biosynthesis protein 4 homolog（COQ4）in mammals by using Coq4 knockout（Coq4^-/- ）mice. Methods：Coq4 global heterozygous mouse models were introduced，and the different genotypes of mice were detected by genomic PCR. The phenotypes，growth，reproduction of Coq4 ^+/- mice were observed and recorded. The morphology and structure of embryonic and placental tissues of wild type（WT）and Coq4^-/- mice were studied by anatomic and histological analyses as well as immunofluorescence assay. Results：Coq4^-/- mice exhibited an impaired gastrulation on embryonic day （E）7.5（E7.5）and were died on E10.5. Morphological analysis showed severely retarded embryonic development with obvious defective placental structures in Coq4^-/- mice，compared with the WT mice. Immunofluorescence analysis revealed that trophoblast cell invasion was diminished in the placenta of Goq4^-/- mice. Conclusion：Knockout of Coq4 gene leads to impaired placenta and gastrula formation in mice. Coq4 is essential for embryonic development.

Abstract:Objective：To explore the effects of S100A9 knockout on mice with lupus nephritis（LN）induced by pristane，and clarify specific roles of S100A9 in LN. Methods：Ten female wild-type（WT）C57BL/6（B6）mice and ten S100A9^-/- B6 mice（6-8 weeks old） were used. Five WT B6 mice and five S100A9^-/- B6 mice were intraperitoneally injected with 0.5 mL pristane，respectively，serving as experimental groups. Other five WT B6 mice and five S100A9^-/- B6 mice were intraperitoneally injected with 0.5 mL normal saline， respectively，serving as control groups. The mice were sacrificed at six months after injection. The expression of anti-double-stranded DNA（ds-DNA）antibody was measured by ELISA. The levels of serum creatinine，serum urea nitrogen and urine protein were detected. Renal tissues were collected for HE staining to evaluate renal pathology. Results：There were no significant differences between WT and S100A9^-/- B6 mice on mouse body-weight，spleen weight，kidney-structure，and serum creatitine levels etc. Compared with control B6 mice，pristane treated B6 mice showed increased weight and length of spleen as well as increased levels of serum creatinine，urea nitrogen，proteinuria，anti-ds -DNA antibody and IgG，and the lupus -like changes in the kidney with increased glomerular volume， edema or renal tuble epithelium，and stenosis of lumen. Similar results were observed in pristane-treated S100A9^-/- B6 mice，compared with control S100A9^-/- B6 mice. However，compared with pristane -treated WT B6 mice，the above symptoms of LN and indexes of serum and urine were mild in pristane-treated S100A9^-/-B6 mice. Conclusion：Pristane induces systemic lupus erythematosus in B6 mice and S100A9^-/- B6 mice. However，the degree of lesions in mice with S100A9 gene knockout is reduced，suggesting that this gene may have a promoting effect on the pathogenesis of lupus in mice.

Abstract:Objective：To analyze the efficacy of taurochenodeoxycholic acid（TCDCA）on intestinal inflammation and to provide a theoretical basis for the treatment of acute and chronic intestinal inflammation. Methods：In the in vitro and in vitro experiments，the cells and animals were devided into the control group，lipopolysaccharide（LPS）group，and LPS + TCDCA group. In the in vitro experiments，MTT method was firstly applied to screen the appropriate working concentration of TCDCA，and then LPS stimulation was given to the LPS group，and LPS and TCDCA stimulation were given to the LPS + TCDCA group subsequently. The expression of inflammation-related mRNAs and proteins were examined by RT-qPCR and Western blot，respectively . In the in vivo experiments，the LPS group was injected with LPS solution intravenously through the ear margin of rabbits，and the LPS+TCDCA group was treated as above and then fed with TCDCA solution through drinking water. Histopathological alterations of the samples were assessed by HE staining，periodic acid-Schiff staining and Alcian blue-nuclear fast red staining after experimental sampling. Results：The results of in vitro experiments showed that the expression of tumor necrosis factor-α，interleukin-1β，interleukin-6，and interferon-γ indexes was significantly reduced and the expression of interleukin-10 indexes was elevated in macrophages in the LPS+TCDCA group compared with that in the LPS group. In the in vivo experiments，the results of HE staining showed that the inflammation of intestinal tissues was relieved，and the results of periodic acid-Schiff staining and Alcian blue-nucleic solid red staining showed that the number of cup cells and the secretion of acidic as well as neutral mucins in the LPS + TCDCA group increased compared with those in the LPS group. Conclusion：TCDCA alleviates intestinal tissue inflammation and reduces intestinal inflammatory damage caused by LPS by decreasing the expression of inflammatory factors.

Abstract:Objective：To explore the evaluation of myocardial microcirculation characteristics and predictive value for left ventricular remodeling in patients with myocardial infarction using three-dimensional speckle tracking imaging. Methods：A total of 165 patients with myocardial infarction admitted to Chest Hospital affiliated to Zhengzhou University from August 2020 to August 2023 were selected for the study. According to the increase rate of left ventricular end-diastolic volume index（ΔLVEDVI），the patients were divided into left ventricular remodeling group（ΔLVEDVI>20%，74 cases）and non-left ventricular remodeling group（ΔLVEDVI≤20%， 91 cases）. The predictive value of myocardial microcirculation characteristics for left ventricular remodeling in patients with myocardial infarction was evaluated using receiver operating characteristic（ROC）curve. The influencing factors of left ventricular remodeling in patients with myocardial infarction were screened by stepwise regression analysis. A risk prediction model for left ventricular remodeling in patients with myocardial infarction was established and validated. Results：Coronary intervention time，myocardial infarction area，C-reactive protein（CRP），matrix metalloproteinase-（9 MMP-9），vascular endothelial growth factor-A（VEGF-A），index of microcirculatory resistance（IMR），fractional flow reserve（FFR），and coronary flow reserve（CFR）were all independent risk factors affecting left ventricular remodeling in patients with myocardial infarction（P < 0.05）. The calibration curve results showed that the multivariate logistic regression model had good accuracy. Conclusion：Myocardial microcirculation characteristics in patients with myocardial infarction have certain predictive value for left ventricular remodeling.

Abstract:Objective：To explore the relationship between carotid intima -media thickness（cIMT）and subclinical left ventricular function in population of Danyang community. Methods：The study subjects were recruited in 2021 from the Station Community of Danyang City，Jiangsu Province. cIMT was measured and analyzed by GE Vivid E90 ultrasound instrument. Two-dimensional（2D） speckle tracking technology was used to collect left ventricular global longitudinal strain（LVGLS）of the left ventricle as an indicator for assessing subclinical systolic function. The e’and E/e’ratio were obtained from mitral valve blood flow spectra and tissue Doppler imaging，serving as indicators for evaluating subclinical diastolic function. Results：A total of 561 participants with an average age of （58.2 ± 11.7）years were enrolled，among whom 339（60.4% ）were females. Using tertiles of cIMT as a categorical variable，in univariate analysis，LVGLS，E/A ratio，and e’decreased as cIMT tertiles increased，while the E/e’ratio increased（all P_trend ≤ 0.002）， except for left ventricular ejection fraction. However，after further multivariate adjustment，only LVGLS continued to decrease with increasing cIMT tertiles（P < 0.05）. Continuous variable analysis after natural logarithm transformation of cIMT yielded results similar to categorical variable analysis，with only LVGLS showing a significant negative correlation with cIMT（r=- 0.087，P=0.041），and similar findings were observed in regression analysis（β =- 1.12，P=0.041）. Conclusion：In the Danyang community population in Jiangsu，increased cIMT is independently correlated with decreased GLS.

Abstract:Objective：To investigate the peripheral blood lymphocyte subsets and cytokine expression levels in newly diagnosed acute myeloid leukemia（AML）patients with FMS like tyrosine kinase 3 receptor（FLT3）mutations，and their correlation with blood cell counts and mutation types. Methods：A total of 168 AML patients with FLT3 mutations were included in the study. The FLT3 mutation types were further classified，and the lymphocyte subsets，cytokines and blood cell count in peripheral blood of patients before treatment were collected to analyze their correlation. Results：Compared with the healthy control group，the expression levels of CD4， interleukin 6（IL-6），and IL-10 in peripheral blood of patients with FLT3 mutations were increased before treatment，while the expression levels of CD8，CD16 + CD56，IL-2，tumor necrosis factor（TNF），and interferon gamma（IFN-γ）were decreased. According to leukocyte count，the distributions of CD3，CD4，CD8，CD19，IL-4 and IL-10 were different among the groups（P=0.039， P=0.024，P=0.034，P=0.008，P=0.048，P=0.024）. According to platelet count，the distributions of CD19，CD16+CD56 were different among groups（P=0.030，P=0.045）. It can be divided into FLT3-ITD⁺ 、FLT3-TKD⁺ 、FLT3-（ ITD⁺ +TKD⁺ ）and FLT3-（ ITD^- +TKD^- ）.The distributions of CD3，CD8，CD19，IL-10 and TNF were different among the four groups（P=0.046，P=0.048，P=0.041，P=0.042， P=0.013）. Conclusion：The blood cell counts and FLT3 mutation types of AML patients are associated with the expression levels of lymphocyte subsets and cytokines. This may contribute to the risk stratification of AML and have a certain impact on the prognosis of AML patients.

Abstract:Objective：To explore the impact of different body mass index（BMI）ranges of gestational diabetes mellitus（GDM） pregnant women with normal pre-pregnancy BMI on pregnancy outcomes. Methods：A retrospective collection of 2，319 cases of GDM pregnant women with normal pre -pregnancy BMI from May 2022 to May 2023 at Nanjing Maternal and Child Health Hospital. They were divided into Group A（18.5 kg/m² ≤BMI<20.0 kg/m² ，581 cases），Group B（20.0 kg/m² ≤BMI<22.0 kg/m² ，922 cases），and Group C （22.0 kg/m² ≤BMI<24.0 kg/m² ，816 cases）according to pre-pregnancy BMI. Logistic regression was used to analyze and evaluate the association between different BMI levels and pregnancy outcomes. Results：The risk of GDM A2 level，preeclampsia，macrosomia，and neonatal hyperbilirubinemia in the three groups of GDM patients increased with the increase of pre-pregnancy BMI；the risk of placental abruption and neonatal hypoglycemia decreased with the increase of pre-pregnancy BMI. In the normal BMI population， higher or lower pre-pregnancy BMI levels in GDM women are independent risk factors for GDM A2 level，preeclampsia，macrosomia， neonatal hyperbilirubinemia，placental abruption，and neonatal hypoglycemia. Conclusion：Early weight management may be one of the key measures to prevent adverse pregnancy outcomes in GDM pregnant women.

Abstract:Objective：To explore the correlation between blood pressure variability（BPV）and vascular endothelial function induced by nocturnal hypoxia events in obstructive sleep apnea（OSA）patients. Methods：Between February 2022 and April 2023，a total of 131 moderate to severe OSA patients were studied from the departments of Sleep Medicine Centers in three different hospitals， including the Affiliated Huai’an No.1 People’s Hospital of Nanjing Medical University，etc. Continuous non-invasive blood pressure （BP）monitoring was performed simultaneously during polysomnography（PSG）to calculate BPV induced by hypoxic events，the gap between the peak value of systolio blood pressure（SBP）and the lowest SBP during a hypoxia event reflects the amplitude of BP fluctuation（ΔBP）；the number of times ΔBP≥10 mmHg per hour/oxygen desaturation index（ODI）indicates the percentage of hypoxia-induced BP fluctuation. Endothelial function was assessed by flow -mediated dilation（FMD），and patients were divided into normal endothelial function group（n=70）and endothelial dysfunction group（n=61）according to the FMD value. The study analyzed and compared the BPV parameters between the two groups，aiming to explore the factors associated with BPV. Results：There were no significant differences between the two groups of patients in age，sex distribution，body mass index，and OSA severity. Compared with the normal endothelial function group，the endothelial dysfunction group exhibited higher Bnocturnal systolic peak BP［（152.0±7.2） mmHg vs.（148.1±8.8）mmHg］，nocturnal diastolic peak BP［（89.8±5.7）mmHg vs.（87.5±6.6）mmHg］，ΔBP［（15.3±2.9）mmHg vs. （13.3±2.7）mmHg］，the percentage of BP fluctuation［（63.5±14.3）% vs.（44.8±10.7）%，all P < 0.05］，a n d endothelin-1［（50.7± 7.0）ng/L vs.（47.8 ± 8.5）ng/L，P < 0.05］. After adjusting the baseline data of patients，the line regression model showed that the nocturnal SBP peak，the percentage of BP fluctuation，and ΔBP were all positively correlated with FMD（all P < 0.05）. Conclusion：For moderate-to-severe OSA patients，the elevation of BPV induced by nocturnal hypoxia events is closely correlated to vascular endothelial dysfunction.

Abstract:Objective：To analyze the long-term trend of height growth at the age of 17 among 18 ethnic minority students in China from 1985 to 2019. Methods：Seven reports on the physical fitness and health of Chinese students（except for 1991）were extracted to study the average height of 18 ethnic minority students in China，including Mongolian，Hui，Uyghur，Zhuang，Korean，Tibetan，Miao， Buyi，Dong，Bai，Tujia，Hani，Dai，Lisu，Wa，Naxi，Tu，and Qiang. Results：The average height of 17-year-old boys from eaeh ethnic minorities increased significantly over the past 34 years（P < 0.05）. In 2019，among the 18 ethnic minority boys aged 17，the Hui boys had the highest average height（173.09 cm），while the Miao boys had the lowest average height（162.66 cm）. The Ethnic groups with a height increase of over 1 cm every 10 years included Dong（1.96 cm/10 years），Bai（1.96 cm/10 years），Tujia（1.95 cm/10 years），Qiang （1.80 cm/10 years），Hui（1.80 cm/10 years），Mongolian（1.79 cm/10 years），Tu（1.72 cm/10 years），Uyghur（1.63 cm/10 years）， Tibetan（1.61 cm/10 years），Buyi（1.55 cm/10 years），Naxi（1.52 cm/10 years），Dai（1.35 cm/10 years），Lisu（1.29 cm/10 years），Hani （1.25 cm/10 years），Zhuang（1.16 cm/10 years），and Wa（1.06 cm/10 years）. The ethnic group with a height increase of less than 1 cm every 10 years is Miao（0.95 cm/10 years）. In 2019，among 18 ethnic minority girls aged 17，the average height of Hui girls was the highest（161.71 cm），while Buyi girls had the lowest average height（151.63 cm）. The ethnic groups with a height increase of over 1 cm every 10 years were Tujia（1.80 cm/10 years），Hui（1.52 cm/10 years），Tu（1.25 cm/10 years），Bai（1.23 cm/10 years），Dong（1.18 cm/ 10 years），Chinese Korea（1.12 cm/10 years），and Qiang（1.04 cm/10 years）. Over the 34 years，except for Oyghur and Miao，the height of girls from 16 other ethic minorities increased significantly（P < 0.05）. Conclusion：All male ethnic minority students in China have shown a significant long-term growth trend，while most female ethnic minority students have shown a significant long-term growth trend. The uneven height growth of male and female students from different ethnic groups proves that the growth potential of minority students from different regions and ethnic groups in China can be fully realized，and higher attention needs to be paid to ethnic groups with slower height growth，and for those ethnic groups with rapid height growth，it is also necessary to prevent the negative effects it brings.

Abstract:Pancreatic cancer is a highly lethal and aggressive tumor that affects the digestive tract，leading to poor prognosis and low survival rate. At present，gemcitabine-based chemotherapy is widely used in the clinical treatment of pancreatic cancer. However，the efficacy of chemotherapy has significantly decreased with the emergence of clinical drug resistance. In order to meet its demand of energy and biological materials，tumors always change its metabolic pathway，which is called tumor metabolic reprogramming. The abnormal enhancement of aerobic glycolysis is one of characteristics of glucose metabolic reprogramming in pancreatic cancer cells. The glucose transporter proteins and key enzymes are participated in the processes and regulated chemotherapy resistance through different signal pathways. The purpose of this study is to summarize the relationship between drug resistance and glucose metabolic reprogramming in pancreatic cancer. The mechanisms and regulatory signaling pathways are also analyzed. Furthermore，the pre-clinical trials and drug development targeting the glycolysis metabolic pathways are summarized and analyzed.

Abstract:The life activities of organisms are controlled and regulated by proteins，and the vast majority of proteins exert their function through interactions with other proteins. This article briefly describes research methods for detecting interactions of proteins based on principles of biochemistry and molecular biology，biophysics，and bioinformatics，and reviews the characteristics of these methods.

Abstract:Adenine nucleotide translocases（ANTs）are crucial for mitochondrial integrity and bioenergetic metabolism. There are four isoforms of ANTs. Under physiological conditions，ANTs primarily engage in the exchange of adenosine diphosphate（ADP）and adenosine triphosphate（ATP）across mitochondrial membranes. ANT isoforms are also potentially significant components of the mitochondrial permeability transition pore（mPTP），contributing to processes such as cellular apoptosis and proton leakage. Impairment of ANTs leads to mitochondrial dysfunction，which holds significant pathological implications in metabolic diseases， cardiomyopathies，and cancer progression. This review summarizes recent advancements and knowledge regarding ANTs，aiming to offer new insights into potential therapeutic strategies targeting ANTs in diseases.

Abstract:Gynecological malignancies，such as cervical cancer，ovarian cancer，and endometrial cancer，are characterized by a high degree of heterogeneity. Once they enter the advanced stage，the prognosis is often poor. The emergence and development of single-cell sequencing technology have provided a better platform for investigating the mechanisms of tumor initiation and progression，identifying rare cells，mapping cellular lineages，guiding targeted precision therapies for tumors，and predicting patient outcomes at the single-cell level. This article provides a comprehensive review of the rise and development of single-cell sequencing technology and its applications in the research on gynecologic malignancies.

Abstract:Lipoxin A₄（LXA₄）is a natural pro -catabolic molecule produced by endogenous fatty acids that is known as the“brake signal”of inflammatory factors. It has a powerful anti-inflammatory effect，but its metabolism is fast，and LXA₄ analogues are relatively more stable and also have certain anti-inflammatory effects. The star cell in the fight against inflammation，the macrophage，is a vital component of our natural immunological barrier and plays a crucial role in inflammation reduction，as does LXA₄. LXA₄ and its analogs are intricately related to macrophages in the anti-inflammatory process. The interactions between the two in the inflammatory response are examined in order to generate novel ideas for treating a variety of inflammation-related disorders.

Abstract:Obesity is caused by excessive energy intake and reduced consumption，when the energy intake exceeds the containing capacity of adipose tissue（AT），AT undergoes functional disorders and triggers a series of metabolic related changes. Thyroid gland， being the key organ regulating the energy metabolism of the body，it exerts an profound influence on the adipose tissue，the main energy storage organ. It can regulate the glucose and lipid metabolism，mitochondrial function and phenotype change of adipose tissue through direct and indirect effects，and has an indispensable impact on the occurrence and development of obesity and metabolic syndrome. In the past，researches on thyroid and fat mostly focused on the unilateral effect of thyroid on adipose tissue，while it’s been recently pointed out that adipose tissue can also affect thyroid function through lipotoxicity，secretion of adipokine and proinflammatory factors， leading to thyroid diseases such as thyroid nodules，thyroid dysfunction. This article describes the interaction between thyroid and adipose tissue and its role in the occurrence and development of obesity related diseases and thyroid related diseases.

Abstract:Exosome-derived microRNAs（miRNA）are a class of non-coding single-stranded RNA secreted by exosomes，which alter protein expression by inhibiting the translation of messenger RNA. In diabetes，alterations in the coding regions of genes lead to changes in miRNA expression. These variations induce a series of pathophysiological changes，such as oxidative stress，mitochondrial dysfunction，myocardial apoptosis and pyroptosis，vascular remodeling，and fibrosis，thereby participating in the occurrence and development of diabetic heart disease. This article reviews the characteristics of exosome-derived miRNAs and summarizes their roles and therapeutic potential in diabetic heart disease.

Abstract:Chronic obstructive pulmonary disease（COPD），the third leading cause of death worldwide，is a chronic inflammatory airway disease characterized by incompletely reversible airflow limitations. The pathogenesis of COPD is complex，and the specific mechanisms are still unclear. Extracellular vesicles（EVs），including exosomes，microvesicles（MVs），and apoptotic bodies（ABs）， carry various proteins，lipids，DNA，mRNA and microRNA，and other cell-derived components，participating in processes such as intercellular communication，cell migration，angiogenesis，and immune regulation. In recent years，the role of EVs in pulmonary diseases has attracted significant attention. This article provides a review of recent studies on the relationships between EVs and COPD.

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