Primary cilia—those solitary, microtubule-based projections extending from the surface of most eukaryotic cells—are increasingly recognized not merely as cellular appendages, but as sophisticated signaling hubs. By compartmentalizing specific receptors (e.g., GPCRs) and effectors within a microdomain guarded by the transition zone, these organelles function effectively as high-gain sensors capable of integrating mechanical stimuli with metabolic cues. In this review, we examine the pivotal role of primary cilia across the nervous, bone-vascular, and renal landscapes, arguing for a unified “mechano-metabolic coupling” framework. Here, conserved ciliary modules are not static; rather, they are differentially deployed to uphold systemic homeostasis. Within the central nervous system, we position primary cilia as upstream integrators. We highlight how hypothalamic neuronal cilia concentrate metabolic receptors, such as the melanocortin 4 receptor (MC4R), to interpret energy status. Moreover, the recent identification of serotonergic “axon-cilium synapses” points to a direct mode of neurotransmission, wherein 5-HT6 receptors drive nuclear signaling and chromatin accessibility to rapidly modulate gene expression. Through these mechanisms, central cilia modulate sympathetic tone and neuroendocrine output, effectively establishing the mechanical and metabolic “boundary conditions” under which peripheral organs operate. Dysfunction in these central hubs is linked to obesity and neurodevelopmental disorders, including Bardet-Biedl syndrome. In peripheral tissues, cilia serve as versatile mechanotransducers that convert physical forces into biochemical responses. Regarding the bone-vascular system, we discuss the translation of mechanical loads and fluid shear stress into structural remodeling. In osteoblasts, specifically, ciliary integrity is intrinsically linked to cholesterol and glucose metabolism, fine-tuning the balance between Hedgehog and Wnt/β-catenin signaling to govern osteogenesis and bone repair. A similar dynamic exists in the vasculature, where endothelial cilia sense shear stress to modulate KLF4 expression and endothelial-to-mesenchymal transition—processes critical for valvulogenesis and vascular remodeling. Meanwhile, in the kidney, tubular cilia act as terminal effectors within a “shear-cilia-metabolism” axis. Here, fluid shear stress engages ciliary signaling to trigger AMPK-mediated lipophagy and mitochondrial biogenesis, thereby securing the ATP supply required for solute transport. Notably, dysregulation of this axis leads to metabolic reprogramming and aberrant proliferation, acting as a hallmark driver of cystogenesis in polycystic kidney disease (PKD). Crucially, this review attempts to dissect the often-conflated logic of cross-system integration by distinguishing 3 non-equivalent pathways: direct communication via ciliary extracellular vesicles, though this remains largely hypothetical in long-range signaling; “physiology-mediated cascades”, where ciliary dysfunction in a single organ—such as the kidney—precipitates systemic pathology through hemodynamic and metabolic shifts (e.g., altered blood pressure, fluid volume, or uremic toxins); and “parallel molecular defects”, where shared genetic mutations in ubiquitous components like the IFT machinery cause simultaneous, independent failures across multiple organ systems. Building on these distinctions, we propose a nested-loop model that links central set-points with peripheral feedback via physiological variables. Furthermore, we construct a “causality-to-translation” roadmap that pinpoints structural repair (e.g., targeting IFT assembly) and metabolic rescue (e.g., AMPK activation or autophagy induction) as promising therapeutic avenues. Ultimately, this framework provides a theoretical basis for deciphering the shared pathological mechanisms of multisystem ciliopathies, offering a strategic guide for the development of targeted interventions that go beyond symptomatic treatment.

Natural products are an important source for innovative drugs,but unclear molecular targets and mechanisms limit their further development and application.The authors proposed a new method for the target identification of natural products based on proteolysis-targeting chimera(PROTAC)technology and quantitative proteomics,and established the targeted degradomics(TGDO) technology for the identification of weak-affinity tar-gets.This article summarizes the standardized workflow and the application of TGDO for target identification of natural products.

The application of sensors to the monitoring of spinal morphology and motion was reviewed in terms of the research object and monitoring index.The present situation of the application of sensors was introduced,such as inertial sensor,stretchable strain sensor and electromagnetic sensor.The deficiencies of sensors applied to the monitoring of spinal morphology and motion were analyzed,and the future directions of the application were pointed out.[Chinese Medical Equipment Journal,2025,46(6):105-110]

To investigate the antimicrobial resistance of Enterococci isolated from 596 anal swabs,feces and environmental samples were collected from pig,cattle,chicken and quail farms in Chang-sha,Hunan Province,Enterococci were isolated and identified by mass spectrometry.The minimum inhibitory concentrations(MICs)of 10 antimicrobial agents were determined by AGAR diffusion method.Whole genome sequencing(WGS)was used to detect the distribution of multilocus se-quence typing(ST),drug resistance genes and virulence genes.A total of 272 strains of Enterococ-cus were isolated(45.6％).The isolates were resistant to cefoxitin(68.9％)and cefotiofur(58.5％),followed by trimethoprim/sulfamethoxazole(52.2％),vancomycin(4.4％),and linezolid(13.6％).In this study,six linezolid highly resistant Enterococci isolates were analyzed by whole genome sequencing to explore the transmission mechanism of linezolid resistance because linezolid is forbidden to be used in aquaculture.ST403(4/6),ST16(1/6)and ST476(1/6)were the most common ST types,which all originated from the same farm.Three oxazolidinone resistance genes(cfr,poxtA and optrA)were found in all 21 strains.One strain(Ecc60)carried all three oxazo-lidinone resistance genes,but none of them were located on the plasmid.tet(M),aph(3')-Ⅲ,and lsa(A)were found in all six Enterococcus isolates.Interestingly,the present study is the first to i-dentify enterococci carrying the optrA gene in quail fecal samples.The analysis of the genetic envi-ronment of oxazolidinone resistance genes showed that the genetic environment of cfr(D),poxtA and optrA of isolates from the same farm was similar.A total of 19 virulence genes were detected in 6 isolates,of which 12 genes(ElrA,SrtA,ace,agg,cCF10,cOB1,cad,camE,ebpA,ebpC,efaAfs,tpx)were carried by all 6 isolates,and the types of virulence genes in strains from the same farm were extremely similar.The results showed that the drug resistance of Enterococci iso-lated from the fish farms in Changsha was serious,and the resistance rate to linezolid,which was prohibited in the fish farms,was high.The oxazolidinone resistance gene loci were accompanied by other resistance genes,especially the florfenicol resistance gene(FexA),which may be related to the abuse of florfenicol in the fish farms.

Objective To investigate the clinical efficacy and safety of facilitated percutaneous coronary intervention(PCI)with half-dose recombinant staphylokinase(r-SAK)in patients with ST-segment elevation myocardial infarction(STEMI)who are expected to undergo PCI within 120 minutes.Methods From October 2021 to August 2022,a total of 200 STEMI patients in eight centers were included and randomly assigned in a 1﹕1 ratio to either r-SAK group or control group.Patients received loading doses of aspirin and ticagrelor and intravenous heparin and were randomized to receive an intravenous bolus of either 5 mg r-SAK or normal saline prior to PCI.The outcomes were set as ST-segment resolution(STR)at 60-90 minutes after PCI,the proportion and transition of pathological Q waves on the 5th day after PCI,and the proportion of high-sensitivity cardiac troponin T(hs-cTnT)peaking within 12 hours of onset.The safety outcome was major bleeding events defined as Bleeding Academic Research Consortium(BARC)≥type 3 bleeding during hospitalization.Results Compared with the control group,the r-SAK group had a higher proportion of STR≥70%within 60-90 minutes after PCI(58.3%vs.40.3%,P=0.009);a lower proportion of pathological Q waves(59.1%vs.74.1%,P=0.040);a lower rate of Q wave progression(14.8%vs.43.2%,P＜0.001);a higher rate of Q wave disappearance(12.5%vs.3.7%,P=0.027);and a higher proportion of hs-cTnT peaking within 12 hours of symptom onset[31/40(77.5%)vs.17/33(51.5%),P=0.027].Regarding the safety outcome,no significant difference in BARC≥type 3 bleeding was found between the two groups during hospitalization(P＞0.05).Conclusions For STEMI patients who were expected to undergo primary PCI within 120 minutes of symptom onset,the facilitated PCI with half-dose r-SAK significantly increased the proportion of STR≥70%at 60-90 minutes after PCI,reduced the formation of pathological Q waves,and shortened the time to peak hs-cTnT,without increasing the risk of bleeding,which should be an alternative reperfusion strategy worthy of further study.

High myopia is a refractive abnormality characterized by excessive elongation of the eye axis.The sclera,as an important part of the eye axis regulation,plays a key role in the occurrence and development of high myopia.In this pa-per,based on the domestic and international articles,the pathological changes and related regulatory molecules of the scle-ra in high myopia were systematically summarized from the features of scleral lesions in high myopia and the gene regula-tion and signaling pathways affecting the ultrastructure and mechanical properties of the sclera,thus providing a theoretical basis for the study of the pathological mechanism of high myopia.

Objective To investigate the role of Insulin like growth factor 2 mRNA binding protein 1(IGF2BP1)and long non-coding RNA LINC00160(LINC00160)in gastric cancer,and its potential mechanism of regulating the proliferation and invasion of gastric cancer cells.Methods Quantitative real time polymerase chain reaction(qRT-PCR)was used to detect the expression level of LINC00160 in gastric cancer tissues and cells.Bioinformatics prediction,RNA-binding protein immunoprecipitation(RIP)and methylated RNA immunoprecipitation(MeRIP)were used to verify the binding effect of LINC00160 and IGF2BP1.The correlation between the expression of LINC00160 and IGF2BP1 in gastric cancer tissues was analyzed by Pearson assay.CCK-8 assay and Transwell assay were used to detect cell proliferation and invasion.The changes of aerobic glycolysis index[glucose intake,lactate production,and Adenosine-triphosphate(ATP),extracellular acidification rate(ECAR)and oxygen consumption rate(OCR)]were detected and analyzed.Results Compared with normal tissues,the expression of LINC00160 in gastric cancer tissues(5.13±0.62 vs 1.02±0.03)was significantly up-regulated,and the difference was statistically significant(t=-36.266,P<0.001).The expression level of LINC00160 in gastric cancer cells was higher than that of human normal gastric epithelial cell line GES-1,and the difference was statistically significant(F=24.595,P<0.001).Compared with the control group,silenting LINC00160 significantly inhibited the proliferation(0.42±0.03 vs 1.03±0.04)and invasion(22.13%±1.97%vs 42.15%±2.67%)of AGS cells,decreased glucose uptake(2.11±0.26mmol/L vs 4.22±0.37mmol/L)and lactate production(6.84±1.25mmol/L vs 11.68±1.55mmol/L),decreased ECAR,and increased ATP(3.34±0.29mmol/L vs 1.87±0.24mmol/L)levels and OCR,and the differences were statistically significant(t=4.188～24.423,all P<0.01).The expression of IGF2BP1 protein in gastric cancer tissues(4.07±0.36)was significantly higher than that in adjacent tissues(1.01±0.03),and the difference was statistically significant(t=-46.396,P<0.01),and was positively correlated with the expression of LINC00160(r2=0.774 5,P<0.01).Mechanistic studies revealed that IGF2BP1 upregulated LINC00160 expression by binding m6A modified LINC00160 to promote its stability.Silencing IGF2BP1 significantly inhibited the expression of LINC00160 and the proliferation,invasion and aerobic glycolysis of gastric cancer cells,and the differences were statistically significant(t=4.386～11.989,all P<0.01).Overexpression of LINC00160 reversed the effect of IGF2BP1 silencing on AGS cells.Conclusion LINC00160 is significantly up-regulated in gastric cancer,and IGF2BP1 may stably regulate the expression of LINC00160 through m6A modification,promote the aerobic glycolysis of tumor cells,and participate in the occurrence and development of gastric cancer.

Objective:To explore the effect of Wuqinxi combined with resistance training on cardiac function and self-care ability in patients with chronic heart failure(CHF).Methods:This randomized controlled study enrolled 152 CHF patients admitted to Nanjing Hospital of Chinese Medicine between September 2018 and December 2022.Pa-tients were divided into control group(n=76)and intervention group(n=76).Patients in control group received routine intervention measure combined resistance training,while those in the intervention group received additional Wuqinxi.Both groups were intervened for 6 months.The clinical total effective rate,cardiac function,self-care ability and quality of life were compared between two groups.We also compared the incidence of adverse events and readmission rate during 6-month follow-up.Results:The total effective rate of the intervention group was sig-nificantly higher than that of the control group(93.2％vs.81.1％,P=0.003).Compared with patients in the control group,those in the intervention group had significant higher left ventricular ejection fraction(LVEF)[(50.08±8.37)％vs.(43.47±8.02)％]and 6min walking distance(6MWD)[(496.76±40.54)m vs.(406.76±28.65)m](P＜0.001 both);and significant lower left ventricular end-diastolic volume(LVEDV)[(109.82±9.90)ml vs.(165.29±12.26)ml],left ventricular end-systolic volume(LVESV)[(59.09±2.69)ml vs.(72.61±3.54)ml],score of the European Heart Failure Self-care Behaviour Scale(EHFScBS)[(26.49±3.24)points vs.(35.80±4.33)points],and Minnesota Living with Heart Failure Questionnaire(MLHFQ)total score[(43.78±4.50)points vs.(56.55±4.92)points](P＜0.001 all).The total incidence of adverse events(2.8％vs.12.3％)and readmission rate(1.4％vs.11.0％)in the intervention group were significantly lower than those of the control group(P＜0.05 both).Conclusion:Wuqinxi combined with resistance training may improve clinical efficacy,cardiac function,self-care ability,reduce incidence of adverse events and readmission,then improve quality of life in CHF patients.

Chronic cerebral hypoperfusion leads to white matter injury (WMI), which plays a significant role in contributing to vascular cognitive impairment. While 13-docosenamide is a type of fatty acid amide, it remains unclear whether it has therapeutic effects on chronic cerebral hypoperfusion. In this study, we conducted bilateral common carotid artery stenosis (BCAS) surgery to simulate chronic cerebral hypoperfusion-induced WMI and cognitive impairment. Our findings showed that 13-docosenamide alleviates WMI and cognitive impairment in BCAS mice. Mechanistically, 13-docosenamide specifically binds to cannabinoid receptor 1 (CNR1) in oligodendrocyte precursor cells (OPCs). This interaction results in an upregulation of ubiquitin-specific peptidase 33 (USP33)-mediated CNR1 deubiquitination, subsequently increasing CNR1 protein expression, activating the phosphorylation of the AKT/mTOR pathway, and promoting the differentiation of OPCs. In conclusion, our study suggests that 13-docosenamide can ameliorate chronic cerebral hypoperfusion-induced WMI and cognitive impairment by enhancing OPC differentiation and could serve as a potential therapeutic drug.
Animals ; Oligodendrocyte Precursor Cells/metabolism* ; Mice ; Cell Differentiation/drug effects* ; Male ; Receptor, Cannabinoid, CB1/metabolism* ; Mice, Inbred C57BL ; Ubiquitin Thiolesterase/metabolism* ; Ubiquitination/drug effects* ; Carotid Stenosis/complications* ; Cognitive Dysfunction/drug therapy*