摘要：The macrophage-mediated inflammatory response is crucial for the recovery of skeletal muscle following ischemia.Therefore,macrophage-based therapeutic targets need to be explored for ischemic disease.In the current study,we found that the mRNA levels of scavenger receptor A1(Sr-a1)were elevated in patients with critical limb ischemia,based on an analysis of the Gene Expression Omnibus data.We then investigated the role and underlying mechanisms of macrophage SR-A1 in a mouse hindlimb ischemia(HLI)model.Compared with the Sr-a1fl/fl mice,the LyzCre/+/Sr-a1flox/flox(Sr-a1ΔMΦ)mice showed significantly reduced laser Doppler blood flow in the ischemic limb on day seven after HLI.Consistently,histological analysis revealed that the ischemic limb of the Sr-a1ΔMΦ mice exhibited more severe and prolonged necrotic morphology,inflammation,fibrosis,decreased vessel density,and delayed regeneration than that of the control Sr-a1fl/fl mice.Furthermore,restoring wild-type myeloid cells to the Sr-a1 knockout mice effectively improved the Doppler perfusion in the ischemic limb and mitigated skeletal muscle damage seven days after HLI.Consistent with these in vivo findings,co-cultivating macrophages with the mouse myoblast cell line C2C12 revealed that the Sr-a1-/-bone marrow macrophages significantly inhibited myoblast differentiation in vitro.Mechanistically,SR-A1 enhanced the skeletal muscle regeneration in response to HLI by inhibiting oncostatin M production via suppression of the NF-κB signaling activation.These findings indicate that SR-A1 may be a promising candidate protein to improve tissue repair and regeneration in peripheral ischemic arterial disease.

摘要：Interleukin (IL)-18,a member of the IL-1 family,is commonly known as an interferon-γ inducer and is expressed in both hematopoietic and non-hematopoietic cells,such as intestinal epithelial cells,keratinocytes,and endothelial cells. In the immune system,the mature IL-18 plays a critical role in eliminating tumors and infectious agents by activating NK cells and T-lymphocytes,and by synergizing with other cytokines like IL-12 and IL-1β to induce inflammation[1-2]. However,excessive activation of IL-18 may cause a variety of immune-inflammatory diseases,including psoriasis,atherosclerosis,Alzheimer's disease,and inflammatory bowel disease[3-4]. Regarding the activation mechanism of IL-18,similar to immune cells,mouse non-immune cells rely on caspase-1 for its processing and maturation.However,the activation mechanism of IL-18 in human non-immune cells remains unclear.

摘要：Endometriosis is defined as a condition with endometrium-like tissues migrating outside of the pelvic cavity.However,the mechanism of endometriosis is still unclear.Lactate can be covalently modified to lysine residues of histones and other proteins,which is called lactylation.The results showed that the higher level of lactate and lactate dehydrogenase A enhanced the histone H3 lysine 18 lactylation(H3K18lac)in ectopic endometrial tissues and ectopic endometrial stromal cells than that in normal endometrial tissues and normal endometrial stromal cells.Lactate promoted cell proliferation,migration,and invasion in endometriosis.Mechanistically,lactate induced H3K18lac to promote the expression of high-mobility group box 1(HMGB1)in endometriosis,and HMGB1 knockdown significantly reduced the cell proliferation,migration,and invasion of the lactate-treated cells through the phosphorylation of AKT.In conclusion,lactate could induce histone lactylation to promote endometriosis progression by upregulating the expression of HMGB1,which may provide a novel target for the prevention and treatment of endometriosis.

摘要：Inflammation plays a crucial role in the initiation and progression of sepsis and induces alterations in brain neurotransmission,thereby contributing to the development of sepsis-associated encephalopathy(SAE).Parvalbumin(PV)interneurons are pivotal contributors to cognitive processes and have been implicated in various central nervous system dysfunctions,including SAE.Oxytocin,known for its ability to augment the firing rate of gamma-aminobutyric acid(GABA)-ergic interneurons and directly stimulate inhibitory interneurons to enhance the tonic inhibition of pyramidal neurons,has prompted an investigation into its potential therapeutic effects on cognitive dysfunction in SAE.In the current study,we administered intranasal oxytocin to SAE mice induced by lipopolysaccharide.Behavioral assessments,including open field,Y-maze,and fear conditioning,were used to evaluate cognitive performance.Golgi staining revealed hippocampal synaptic deterioration,local field potential recordings showed weakened gamma oscillations,and immunofluorescence staining demonstrated decreased PV expression in the cornu ammonis 1(CA1)region of the hippocampus following lipopolysaccharide treatment,all of which were alleviated by oxytocin administration.Furthermore,immunofluorescence staining of PV co-localization with vesicular glutamate transporter 1 or vesicular GABA transporter indicated a balanced excitation/inhibition effect of neurotransmitters on PV interneurons after oxytocin administration in the SAE mice,leading to an improved cognitive function.In conclusion,oxytocin treatment improved cognitive function by increasing the number of PV+neurons in the hippocampal CA1 region,restoring the balance of excitatory/inhibitory synaptic transmission on PV interneurons,and enhancing hippocampal CA1 local field potential gamma oscillations.These findings suggest a potential mechanism underlying the beneficial effects of oxytocin in SAE.

摘要：Bladder cancer(BC)is the tenth most prevalent malignancy globally,presenting significant clinical and societal challenges because of its high incidence,rapid progression,and frequent recurrence.Presently,cystoscopy and urine cytology serve as the established diagnostic methods for BC.However,their efficacy is limited by their invasive nature and low sensitivity.Therefore,the development of highly specific biomarkers and effective non-invasive detection strategies is imperative for achieving a precise and timely diagnosis of BC,as well as for facilitating an optimal tumor treatment and an improved prognosis.microRNAs(miRNAs),short noncoding RNA molecules spanning around 20-25 nucleotides,are implicated in the regulation of diverse carcinogenic pathways.Substantially altered miRNAs form robust functional regulatory networks that exert a notable influence on the tumorigenesis and progression of BC.Investigations into aberrant miRNAs derived from blood,urine,or extracellular vesicles indicate their potential roles as diagnostic biomarkers and prognostic indicators in BC,enabling miRNAs to monitor the progression and predict the recurrence of the disease.Simultaneously,the investigation centered on miRNA as a potential therapeutic agent presents a novel approach for the treatment of BC.This review comprehensively analyzes biological roles of miRNAs in tumorigenesis and progression,and systematically summarizes their potential as diagnostic and prognostic biomarkers,as well as therapeutic targets for BC.Additionally,we evaluate the progress made in laboratory techniques within this field and discuss the prospects.

摘要：Premature ovarian insufficiency(POI)caused by chemotherapy is a common complication in female cancer survivors of childbearing age.Traditional methods,including mesenchymal stem cell(MSC)transplant and hormone replacement therapy,have limited clinical application because of their drawbacks,and more methods need to be developed.In the current study,the potential effects and underlying mechanisms of human umbilical cord MSC-derived extracellular vesicles(hUCMSC-EVs)were investigated in a cisplatin(CDDP)-induced POI mouse model and a human granulosa cell(GC)line.The results showed that hUCMSC-EVs significantly attenuated body weight loss,ovarian weight loss,ovary atrophy,and follicle loss in moderate-dose(1.5 mg/kg)CDDP-induced POI mice,similar to the effects observed with hUCMSCs.We further found that the hUCMSC-EVs inhibited CDDP-induced ovarian GC apoptosis by upregulating anti-apoptotic miRNA levels in GCs,thereby downregulating the mRNA levels of multiple pro-apoptotic genes.In general,our findings indicate that the moderate-dose chemotherapy may be a better choice for clinical oncotherapy,considering effective rescue of the oncotherapy-induced ovarian damage with hUCMSC-EVs.Additionally,multiple miRNAs in hUCMSC-EVs may potentially be used to inhibit the chemotherapy-induced ovarian GC apoptosis,thereby restoring ovarian function and improving the life quality of female cancer patients.

摘要：Intracranial hemorrhage(ICH)causes numerous neurological deficits and deaths worldwide each year,leaving a significant health burden on the public.The pathophysiology of ICH is complicated and involves both primary and secondary injuries.Hematoma,as the primary pathology of ICH,undergoes metabolism and triggers biochemical and biomechanical alterations in the brain,leading to the secondary injury.Past endeavors mainly aimed at biochemical-initiated mechanisms for causing secondary injury,which have made limited progress in recent years,although ICH itself is also highly biomechanics-related.The discovery of the mechanically-activated cation channel Piezo1 provides a new avenue to further explore the mechanisms underlying the secondary injury.The current article reviews the structure and gating mechanisms of Piezo1,its roles in the physiology/pathophysiology of neurons,astrocytes,microglia,and bone-marrow-derived macrophages,and especially its roles in erythrocytic turnover and iron metabolism,revealing a potential interplay between the biomechanics and biochemistry of hematoma in ICH.Collectively,these advances provide deeper insights into the secondary injury of ICH and lay the foundations for future research.

摘要：Introduction Gender and sex are related to important quality and safety issues in scientific,health,and clinical research.Sex refers to biological characteristics,while gender encompasses the sociocultural norms,identities,and relationships that shape communities and organiza-tions,as well as influence actions,behaviors,contexts,and knowledge. Both gender and sex intersect with other social categories. In this context,in addition to sex or gender,the intersectionality refers to overlapping or interdependent systems of discrimi-nation by more than one factor,such as age,disability,ethnicity,geographic location,socioeconomic status,and sexuality,among others.

摘要：Aberrant alternative polyadenylation(APA)events play an important role in cancers,but little is known about whether APA-related genetic variants contribute to the susceptibility to bladder cancer.Previous genome-wide association study performed APA quantitative trait loci(apaQTL)analyses in bladder cancer,and identified 17 955 single nucleotide polymorphisms(SNPs).We found that gene symbols of APA affected by apaQTL-associated SNPs were closely correlated with cancer signaling pathways,high mutational burden,and immune infiltration.Association analysis showed that apaQTL-associated SNPs rs34402449 C>A,rs2683524 C>T,and rs11540872 C>G were significantly associated with susceptibility to bladder cancer(rs34402449:OR=1.355,95%confidence interval[CI]:1.159-1.583,P=1.33×10-4;rs2683524:OR=1.378,95%CI:1.164-1.632,P=2.03×10-4;rs11540872:OR=1.472,95%CI:1.193-1.815,P=3.06×10-4).Cumulative effect analysis showed that the number of risk genotypes and smoking status were significantly associated with an increased risk of bladder cancer(Ptrend=2.87×10-12).We found that PRR13,being demonstrated the most significant effect on cell proliferation in bladder cancer cell lines,was more highly expressed in bladder cancer tissues than in adjacent normal tissues.Moreover,the rs2683524 T allele was correlated with shorter 3′ untranslated regions of PRR13 and increased PRR13 expression levels.Collectively,our findings have provided informative apaQTL resources and insights into the regulatory mechanisms linking apaQTL-associated variants to bladder cancer risk.

摘要：Reliable molecular biomarkers to predict fertility remain scarce.The current study investigated the potential of testis-specific circBOULE RNAs as biomarkers for male infertility and sperm quality.Using reverse transcription-PCR and real-time reverse transcription-PCR assays,we identified seven circular RNAs from the human BOULE gene in human sperm.We observed that the expression level of circEx3-6 was significantly reduced in asthenozoospermia,while the expression levels of both circEx2-6 and circEx2-7 were decreased in terato-zoospermia,compared with the controls.Furthermore,we demonstrated that the expression level of circEx2-6 was negatively correlated with the sperm DNA fragmentation index,and the expression level of circEx2-7 was correlated with both fertilization and cleavage rates in those treated with the assisted reproductive technologies.Further functional analyses in a transgenic fly model supported the roles of circBOULE RNAs in sperm development and human male fertility.Collectively,our findings support that sperm circBOULE RNAs may serve as diagnostic biomarkers for assessing sperm motility and DNA quality.Therefore,clinical application and significance of sperm circBOULE RNAs in the assisted reproductive technologies warrant further investigation.

摘要：Long noncoding RNA(lncRNA)IDH1 antisense RNA 1(IDH1-AS1)is involved in the progression of multiple cancers,but its role in epithelial ovarian cancer(EOC)is unknown.Therefore,we investigated the expression levels of IDH1-AS1 in EOC cells and normal ovarian epithelial cells by quantitative real-time PCR(qPCR).We first evaluated the effects of IDH1-AS1 on the proliferation,migration,and invasion of EOC cells through cell counting kit-8,colony formation,EdU,transwell,wound-healing,and xenograft assays.We then explored the downstream targets of IDH1-AS1 and verified the results by a dual-luciferase reporter,qPCR,rescue experiments,and Western blotting.We found that the expression levels of IDH1-AS1 were lower in EOC cells than in normal ovarian epithelial cells.High IDH1-AS1 expression of EOC patients from the Gene Expression Profiling Interactive Analysis database indicated a favorable prognosis,because IDH1-AS1 inhibited cell proliferation and xenograft tumor growth of EOC.IDH1-AS1 sponged miR-518c-5p whose overexpression promoted EOC cell proliferation.The miR-518c-5p mimic also reversed the proliferation-inhibiting effect induced by IDH1-AS1 overexpression.Furthermore,we found that RNA binding motif protein 47(RBM47)was the downstream target of miR-518c-5p,that upregulation of RBM47 inhibited EOC cell proliferation,and that RBM47 overexpressing plasmid counteracted the proliferation-promoting effect caused by the IDH1-AS1 knockdown.Taken together,IDH1-AS1 may suppress EOC cell proliferation and tumor growth via the miR-518c-5p/RBM47 axis.

摘要：The retinal pigment epithelium(RPE)is fundamental to sustaining retinal homeostasis.RPE abnormality leads to visual defects and blindness,including age-related macular degeneration(AMD).Although breakthroughs have been made in the treatment of neovascular AMD,effective intervention for atrophic AMD is largely absent.The adequate knowledge of RPE pathology is hindered by a lack of the patients'RPE datasets,especially at the single-cell resolution.In the current study,we delved into a large-scale single-cell resource of AMD donors,in which RPE cells were occupied in a substantial proportion.Bulk RNA-seq datasets of atrophic AMD were integrated to extract molecular characteristics of RPE in the pathogenesis of atrophic AMD.Both in vivo and in vitro models revealed that carboxypeptidase X,M14 family member 2(CPXM2),was specifically expressed in the RPE cells of atrophic AMD,which might be induced by oxidative stress and involved in the epithelial-mesenchymal transition of RPE cells.Additionally,silencing of CPXM2 inhibited the mesenchymal phenotype of RPE cells in an oxidative stress cell model.Thus,our results demonstrated that CPXM2 played a crucial role in regulating atrophic AMD and might serve as a potential therapeutic target for atrophic AMD.

摘要：The current study used multivariable logistic regression analysis to investigate associations between the intake frequencies of 13 food groups(or four diet groups)and infectious diseases.The analysis included 487 849 participants from the UK Biobank,with 75 209 participants diagnosed with infectious diseases.Participants reporting the highest intake frequency of processed meat(odds ratio[OR]=1.096 4,95%confidence interval[CI]:1.062 2-1.131 8)and red meat(OR=1.089 5,95%CI:1.056 3-1.123 9)had a higher risk of infectious diseases,compared with those with the lowest intake frequency.Consuming fish 2.0-2.9 times(OR=0.822 1,95%CI:0.795 5-0.849 6),cheese≥5.0 times(OR=0.882 2,95%CI:0.855 9-0.909 2),fruit 3.0-3.9 servings(OR=0.886 7,95%CI:0.866 1-0.907 8),and vegetables 2.0-2.9 servings(OR=0.937 2,95%CI:0.918 9-0.955 9)per week were associated with a lower risk of infection.Low meat-eaters(OR=0.940 4,95%CI:0.924 3-0.956 7),fish-eaters(OR=0.839 1,95%CI:0.788 7-0.891 9),and vegetarians(OR=0.915 4,95%CI:0.856 1-0.977 8)had a lower risk of infectious diseases,compared with regular meat-eaters.The mediation analysis revealed that glycosylated hemoglobin,white blood cell count,and body mass index served as the mediators in the associations between diet and infectious diseases.The current study indicates that the intake frequency of food groups is a risk factor for infectious diseases,and fish-eaters have a lower risk of infection.

摘要：Studies have shown that differentiated embryo-chondrocyte expressed gene 1(DEC1)promotes osteoblast osteogenesis.To investigate the role of DEC1 in postmenopausal osteoporosis,we used the two genotypes of mice(Dec1+/+and Dec1-/-)to establish an ovariectomy model and found that the bone loss was significantly lower in Dec1-/-ovariectomy mice than in Dec1+/+ovariectomy mice.The expression levels of RUNX2 and OSX were significantly increased in Dec1-/-ovariectomy mice,compared with Dec1+/+ovariectomy mice;however,the expression levels of NFATc1,c-Fos,CTSK,and RANKL/OPG ratio were significantly decreased in Dec1-/-ovariectomy mice,compared with those in Dec1+/+ovariectomy mice.Likewise,DEC1 deficiency also suppressed the expression levels of IL-6 and IL-1β.Further results showed that the mRNA expression levels of Runx2,Osx,and Alp were significantly increased in bone marrow mesenchymal stem cells of Dec1-/-ovariectomy mice,compared with those of Dec1+/+ovariectomy mice.Moreover,the mRNA levels of Il1b,Il6,Tnfa,and Ifng were significantly increased in bone marrow-derived macrophages(BMMs)of Dec1+/+ovariectomy mice,compared with those of Dec1+/+sham mice,but not in Dec1-/-ovariectomy BMMs,when compared with those in Dec1-/-sham BMMs.Additionally,the expression levels of p-IκBα and p-P65 were significantly increased in Dec1+/+ovariectomy BMMs,compared with those in Dec1+/+sham BMMs,but did not increase in Dec1-/-ovariectomy BMMs,compared with those in Dec1-/-sham BMMs.Taken together,DEC1 deficiency inhibited the NF-κB pathway induced by ovariectomy,thereby decreasing cytokines and subsequently inhibiting the decrease of osteo-genesis and the increase of osteoclastogenesis caused by ovariectomy.The findings may provide a novel under-standing of postmenopausal osteoporosis development,and offer potential avenues for the disease intervention.

摘要：Islet beta cells(β-cells)produce insulin in response to high blood glucose levels,which is essential for preserving glucose homeostasis.Voltage-gated ion channels in β-cells,including Na+,K+,and Ca2+channels,aid in the release of insulin.The epithelial sodium channel alpha subunit(α-ENaC),a voltage-independent sodium ion channel,is also expressed in human pancreatic endocrine cells.However,there is no reported study on the function of ENaC in the β-cells.In the current study,we found that α-ENaC was expressed in human pancreatic glandule and pancreatic islet β-cells.In the pancreas of db/db mice and high-fat diet-induced mice,and in mouse islet β-cells(MIN6 cells)treated with palmitate,α-ENaC expression was increased.When α-ENaC was overexpressed in MIN6 cells,insulin content and glucose-induced insulin secretion were significantly reduced.On the other hand,palmitate injured islet β-cells and suppressed insulin synthesis and secretion,but increased α-ENaC expression in MIN6 cells.However,α-ENaC knockout(Scnn1a-/-)in MIN6 cells attenuated β-cell disorder induced by palmitate.Furthermore,α-ENaC regulated the ubiquitylation and degradation of sirtuin 2 in β-cells.α-ENaC also modulated β-cell function in correlation with the inositol-requiring enzyme 1 alpha/X-box binding protein 1(IRE1α/XBP1)and protein kinase RNA-like endoplasmic reticulum kinase/C/EBP homologous protein(PERK/CHOP)endoplasmic reticulum stress pathways.These results suggest that α-ENaC may play a novel role in insulin synthesis and secretion in the β-cells,and the upregulation of α-ENaC promotes islet β-cell dysfunction.In conclusion,α-ENaC may be a key regulator involved in islet β-cell damage and a potential therapeutic target for type 2 diabetes mellitus.

摘要：The intestinal mucosal barrier serves as a vital guardian of the gut health,maintaining a delicate equilibrium between gut microbiota and host immune homeostasis.Gasdermin D(GSDMD),a key executioner of pyroptosis downstream of the inflammasome,has been found to play intricate roles in modulating colitis by influencing intestinal macrophages and regulating mucus secretion from goblet cells.However,the exact nature of the regulatory function of GSDMD in maintaining intestinal immune homeostasis and defending against pathogens remains to be elucidated.In the current study,by using the Citrobacter rodentium infection model,we found that GSDMD played a key role in the defense against intestinal Citrobacter rodentium infection,with high expression levels in intestinal epithelial and lamina propria myeloid cells.Our results showed that GSDMD acted specifically in intestinal epithelial cells to combat the infection,independently of its effects on antimicrobial peptides or mucin secretion.Instead,the resistance was mediated by the N-terminal fragment of GSDMD,highlighting its importance in intestinal immunity.However,the specific mechanism underlying the N-terminal activity of GSDMD in protecting against intestinal bacterial infections requires future investigation.

摘要：The interplay between DNA replication stress and immune microenvironment alterations is known to play a crucial role in colorectal tumorigenesis,but a comprehensive understanding of their association with and relevant biomarkers involved in colorectal tumorigenesis is lacking.To address this gap,we conducted a study aiming to investigate this association and identify relevant biomarkers.We analyzed transcriptomic and proteomic profiles of 904 colorectal tumor tissues and 342 normal tissues to examine pathway enrichment,biological activity,and the immune microenvironment.Additionally,we evaluated genetic effects of single variants and genes on colorectal cancer susceptibility using data from genome-wide association studies(GWASs)involving both East Asian(7 062 cases and 195 745 controls)and European(24 476 cases and 23 073 controls)populations.We employed mediation analysis to infer the causal pathway,and applied multiplex immunofluorescence to visualize colocalized biomarkers in colorectal tumors and immune cells.Our findings revealed that both DNA replication activity and the flap structure-specific endonuclease 1(FEN1)gene were significantly enriched in colorectal tumor tissues,compared with normal tissues.Moreover,a genetic variant rs4246215 G>T in FEN1 was associated with a decreased risk of colorectal cancer(odds ratio=0.94,95%confidence interval:0.90-0.97,Pmeta=4.70×10-9).Importantly,we identified basophils and eosinophils that both exhibited a significantly decreased infiltration in colorectal tumors,and were regulated by rs4246215 through causal pathways involving both FEN1 and DNA replication.In conclusion,this trans-omics incorporating GWAS data provides insights into a plausible pathway connecting DNA replication and immunity,expanding biological knowledge of colorectal tumorigenesis and therapeutic targets.

摘要：Parasitic helminths,taxonomically comprising trematodes,cestodes,and nematodes,are multicellular invertebrates widely disseminated in nature and have afflicted humans continuously for a long time.Helminths play potent roles in the host by generating a variety of novel molecules,including some excretory/secretory products and others that are involved in intracellular material exchange and information transfer as well as the initiation or stimulation of immune and metabolic activation.The helminth-derived molecules have developed powerful and diverse immunosuppressive effects to achieve immune evasion for parasite survival and establish chronic infections.However,they also improve autoimmune and allergic inflammatory responses and promote metabolic homeostasis by promoting metabolic reprogramming of various immune functions,and then inducing alternatively activated macrophages,T helper 2 cells,and regulatory T cell-mediated immune responses.Therefore,a deeper exploration of the immunopathogenic mechanism and immune regulatory mechanisms of helminth-derived molecules exerted in the host is crucial for understanding host-helminth interactions,as well as the development of therapeutic drugs for infectious or non-infectious diseases.In this review,we focus on the properties of helminth-derived molecules to give an overview of the most recent scientific knowledge about their pathogenic and pharmacopeial roles in immune-metabolic homeostasis.

摘要：Menopause is characterized by various physical,mental and emotional symptoms.ERr 731® is a standardized extract from Rheum rhaponticum root and has been clinically studied for its role in reducing menopausal symptoms.The current systematic review and meta-analysis aimed to evaluate the efficacy of ERr 731® supplementation in alleviating the severity of menopausal symptoms.In this review,we searched across three online databases up to March 2023,evaluated the quality of the included studies by the Physiotherapy Evidence Database scale,and assessed the risk of bias by the Cochrane Risk of Bias tool.We then performed a meta-analysis using RevMan software to estimate the pooled mean difference(MD).The study protocol was registered in the Prospective Register of Systematic Reviews(CRD42023416808).After screening and evaluation,we included four high-quality studies(a total of 390 participants;the ERr 731® group:193 participants;the control group:197 participants)in the meta-analysis.The results showed that ERr 731® supplementation significantly reduced the Menopause Rating Scale score(MD:-15.12;P<0.001),compared with control therapy.Sensitivity analysis revealed no effect of individual studies on the overall pooled estimate or overall observed heterogeneity.The current review provides evidence that ERr 731® supplementation is effective in reducing menopause symptoms.Potential bias and high heterogeneity in the results warrant further clinical studies.

摘要：Numerous studies in immunology focus on areas such as cancer immunotherapy,autoimmune disease therapy,neuroimmunoregulation,immune metabolism,and the discovery of novel immune cell subsets. In endocrinology,there is a focus on the prevention and treatment of diabetes,the management of obesity,thyroid disease,kidney disease,metabolic syndrome,osteoporosis,and the application of artificial intelligence in the management of endocrine diseases,etc. In the current special issue,we selected nine papers covering diverse topics,including ocular vascular diseases,systemic lupus erythematosus(SLE),pathogenic and pharmacopeial roles of helminth-derived molecules,sepsis-induced acute lung injury (ALI),intestinal immune homeostasis,diet and infectious diseases,postmenopausal osteoporosis,per-and polyfluoroalkyl substance (PFAS) exposure and liver damage,and targeted therapies for acrodermatitis continua of Hallopeau (ACH).