Diabetic retinopathy (DR) is one of the most prevalent and vision-threatening microvascular complications of diabetes mellitus, yet its pathogenesis extends far beyond vascular injury alone. As the retina is among the most energy-demanding tissues in the body, its neurons, glial cells, pigment epithelial cells, pericytes, and endothelial cells are highly dependent on mitochondrial oxidative phosphorylation to maintain visual signal transduction, ionic homeostasis, and neurovascular integrity. This review summarizes current evidence indicating that mitochondrial dysfunction is not merely a downstream consequence of chronic hyperglycemia, but a central pathogenic hub that initiates, amplifies, and perpetuates retinal neurovascular degeneration in DR. Persistent hyperglycemia activates multiple abnormal metabolic pathways, including the polyol pathway, hexosamine pathway, protein kinase C signaling, advanced glycation end-product formation, and angiotensin II-related responses. Although these pathways differ mechanistically, they converge on excessive reactive oxygen species (ROS) generation, antioxidant depletion, and mitochondrial injury. Under diabetic stress, electron transport chain overload promotes mitochondrial ROS leakage, damages mitochondrial DNA, disrupts membrane potential, and impairs the transcription of key respiratory chain components. In parallel, mitochondrial quality-control systems become progressively compromised. The balance between fusion and fission shifts toward pathological fragmentation through reduced MFN1/2 and OPA1 activity and enhanced DRP1-mediated fission. Mitochondrial biogenesis is suppressed through inhibition of the AMPK/SIRT1/PGC-1α/NRF1/TFAM axis, while mitophagy changes from an early compensatory response to a later state of autophagic flux blockade and accumulation of dysfunctional mitochondria. Importantly, damaged mitochondria serve as signal amplifiers linking metabolic stress to inflammation and programmed cell death. Mitochondrial ROS, oxidized mitochondrial DNA, calcium overload, cardiolipin exposure, and membrane permeabilization activate interrelated death pathways, including intrinsic apoptosis, ferroptosis, and pyroptosis. Cytochrome C and apoptosis-inducing factor promote caspase-dependent and caspase-independent apoptosis; iron dyshomeostasis, glutathione depletion, GPX4 dysfunction, and lipid peroxidation drive ferroptosis; and mitochondrial danger signals activate the NLRP3 inflammasome and gasdermin-dependent pyroptosis. These pathways jointly damage the retinal neurovascular unit and contribute to pericyte loss, endothelial barrier breakdown, Müller cell dysfunction, retinal ganglion cell apoptosis, retinal pigment epithelial injury, and photoreceptor degeneration. This review also emphasizes the role of epigenetic regulation in stabilizing mitochondrial pathology. DNA methylation, histone modifications, and non-coding RNAs interact to silence mitochondrial protective genes, alter antioxidant responses, and maintain the “metabolic memory” of DR even after glycemic normalization. Therefore, mitochondrial dysfunction should be understood as a dynamic, multidimensional network rather than a single pathological event. Current clinical approaches, such as laser photocoagulation, intravitreal anti-VEGF therapy, and vitrectomy, mainly target advanced vascular lesions and are limited by invasiveness, incomplete responsiveness, recurrence, and potential adverse effects. Therapeutically, strategies targeting mitochondrial ROS, restoring mitochondrial dynamics, enhancing biogenesis, regulating mitophagy, inhibiting inflammasome activation, correcting epigenetic abnormalities, and improving targeted delivery systems show promising potential. However, major translational barriers remain, including retinal cell heterogeneity, stage-specific mitochondrial responses, insufficient organelle-specific drug delivery, and long-term safety concerns. A deeper understanding of mitochondrial regulatory networks may support earlier, more precise, and multi-target interventions for preventing or slowing DR progression.

Purpose To explore the clinical and pathological characteristics of primary benign,borderline,and malignant cardiac tumors in children.Methods 15 cases of primary cardiac tumors in children were collected,and their clinical manifestations,pathological morphology,and immunophenotypes were analyzed.Relevant literature was also reviewed.Results The age of 15 patients ranged from 0.3 to 12 years old,with an average age of about 5 years and a median age of 2 years.9 cases were males and 6 cases were females.4 cases were found to have heart masses during physical examination,3 cases were treated for symptoms of cerebral infarction,1 case was treated for limb weak-ness,1 case was treated for systemic edema,1 case was treated for accelerated heartbeat,1 case was treated for cough,1 case was treated for pneumonia,1 case was treated for abdominal pain,1 case was treated for vomiting,and 1 case was treated for fever and shortness of breath.Echocardiography showed 8 cases occurring in the left heart system(6 in the left atrium and 2 in the left ventricle),4 cases occurring in the right heart system(2 in the right atrium and 2 in the right ventricle),2 cases occurring in the pericardium,and 1 case occurring in the interventricular septum.Ac-cording to pathological diagnosis,13 cases were benign tumors(8 cases of mucinous tumors,4 cases of rhabdomyo-mas,and 1 case of fibroma),1 case was a malignant tumor(embryonal rhabdomyosarcoma),and 1 case was a border-line tumor(NTRK rearranged spindle cell tumor).Conclusion Primary cardiac tumors in children are relatively rare,and borderline and malignant tumors are even rarer.The types of common tumors are different from those in a-dults,and they are prone to misdiagnosis due to non-specific clinical symptoms.For specific cardiac tumors,it is rec-ommended to conduct genetic testing when necessary based on clinical manifestations to further investigate the possibili-ty of related syndromes.

Objective To evaluate the application value of the MR three-dimensional double inversion recovery(3D DIR)sequence in the diagnosis of optic neuritis(ON).Methods A retrospective analysis was conducted on MRI images from 40 patients with sus-pected ON.All patients underwent conventional T2 WI fat suppression(FS)and 3D DIR sequences.The lesion detection rate and diag-nostic accuracy of the intraorbital,intracanalicular,and intracranial segments of the optic nerve were compared between the two sequences,respectively.The receiver operating characteristic(ROC)curves were used to assess the diagnostic performance,and the intraclass correlation coefficient(ICC)were used to analyze interobserver consistency.Imaging assessments were independently performed by two senior and two junior radiologists.Results The sensitivity(SEN),specificity(SPE),and accuracy(ACC)in lesion detection of 3D DIR sequence were significantly better than those of conventional T2 WI FS sequence[odds ratio(OR)221 vs 104,P＜0.001].Notably,3D DIR sequence exhibited superior performance in detecting lesions in the intraorbital segment[area under the curve(AUC)0.915,OR=102]and intracanalicular segment(AUC 0.858,OR=51)compared with conventional T2WI FS sequence.Additionally,3D DIR sequence significantly improved diagnostic consistency among junior radiologists(ICC value increased from 0.469 to 0.655),bring-ing their diagnostic performance closer to that of senior radiologists(AUC improved to 0.883,ACC reached 90.1％).Conclusion The 3D DIR sequence has outstanding diagnostic efficacy in detecting ON lesions,significantly improving ACC and interobserver consistency,thereby offering strong support for the precise diagnosis of ON.

Objective To develop a virtual reality rehabilitation support system and evaluate its effects on improving discharge readiness in caregivers of laryngectomy patients.Methods The system is equipped with a virtual reality-based home nursing skills guidance module for post-laryngectomy patients and an evidence-based artificial intelligence Q&A module.A convenience sampling method was adopted to select 64 caregivers of patients who underwent laryngectomy for the first time in the otorhinolaryngology head and neck surgery department of a tertiary A hospital in Beijing from July 2024 to January 2025 for a systematic study on application effects.To avoid cross-contamination between an experimental group and a control group,ward-based grouping was applied.A coin toss was used to assign Ward 1 to an experimental group and Ward 2 to a control group,with 32 cases in each group.The experimental group received discharge guidance based on the virtual reality technology,while the control group was provided with conventional verbal and written discharge instructions.The readiness for hospital discharge and the quality of discharge teaching scores of caregivers were compared between the 2 groups after the intervention.Results No sample detachment.After the intervention,the patient caregivers in the experimental group scored significantly higher than those in the control group in terms of discharge readiness and quality of discharge guidance,with a statistically significant difference(P＜0.001).Conclusion This study developed the virtual reality rehabilitation system for laryngeal cancer patients demonstrated good feasibility and effectiveness.The application of this system for discharge education significantly improved discharge readiness of caregivers and quality of discharge guidance for post-laryngectomy patients.It also helped with the optimization of health education models,enhancement of nursing resource utilization efficiency,and improvement of transitional care.

Purpose To explore the clinical and pathological characteristics of primary benign,borderline,and malignant cardiac tumors in children.Methods 15 cases of primary cardiac tumors in children were collected,and their clinical manifestations,pathological morphology,and immunophenotypes were analyzed.Relevant literature was also reviewed.Results The age of 15 patients ranged from 0.3 to 12 years old,with an average age of about 5 years and a median age of 2 years.9 cases were males and 6 cases were females.4 cases were found to have heart masses during physical examination,3 cases were treated for symptoms of cerebral infarction,1 case was treated for limb weak-ness,1 case was treated for systemic edema,1 case was treated for accelerated heartbeat,1 case was treated for cough,1 case was treated for pneumonia,1 case was treated for abdominal pain,1 case was treated for vomiting,and 1 case was treated for fever and shortness of breath.Echocardiography showed 8 cases occurring in the left heart system(6 in the left atrium and 2 in the left ventricle),4 cases occurring in the right heart system(2 in the right atrium and 2 in the right ventricle),2 cases occurring in the pericardium,and 1 case occurring in the interventricular septum.Ac-cording to pathological diagnosis,13 cases were benign tumors(8 cases of mucinous tumors,4 cases of rhabdomyo-mas,and 1 case of fibroma),1 case was a malignant tumor(embryonal rhabdomyosarcoma),and 1 case was a border-line tumor(NTRK rearranged spindle cell tumor).Conclusion Primary cardiac tumors in children are relatively rare,and borderline and malignant tumors are even rarer.The types of common tumors are different from those in a-dults,and they are prone to misdiagnosis due to non-specific clinical symptoms.For specific cardiac tumors,it is rec-ommended to conduct genetic testing when necessary based on clinical manifestations to further investigate the possibili-ty of related syndromes.

Objective To investigate the characteristics of Chinese medicine syndromes and the possible metabolic substance basis of spontaneously hypertensive rat(SHR).Methods 10-week-old SPF SHR and WKY of the same strain were divided into SHR group and WKY group with 8 rats in each group.The general state,temperament,peripheral vascular filling,tongue characteristics,diet,water intake,urine and feces volume and characteristics,blood pressure,heart rate,respiratory rate,pain threshold,and open field behavior of SHR rats were observed and tested comprehensively to identify the possible syndrome types of Chinese medicine.At the same time,liquid chromatography tandem mass spectrometry was used to analyze non-targeted serum metabolites to preliminarily reveal the material basis of blood pressure elevation and Chinese medicine syndrome manifestations.Results Compared with WKY group,the scores of dark yellow hair color,irritable degree and peripheral capillary filling were higher in SHR group(P＜0.0001).Red tongue color,dry tongue,little body fluid;24 h diet and water intake,urine volume and fecal volume were less(P＜0.05),fecal water content was lower(P＜0.001);systolic blood pressure(SBP),diastolic blood pressure(DBP),mean arterial pressure(MAP),heart rate(HR)and respiratory rate(RR)were significantly higher(P＜0.05);Lower pain threshold(P＜0.0001);The open field experiment shows that the moving distance and residence time of the edge are longer(P＜0.001).Serum non-targeted metabolomics result showed that,compared with WKY group,the SHR group had 114 metabolites with significant differences(P＜0.05).These differential metabolites were mainly lipids and lipid-like molecules(40.35％),organic acids and derivatives(22.8％),and organoheterocyclic compounds(15.79％).A total of 25 metabolic pathways were identified by KEGG enrichment analysis.Further differential abundance analysis showed that 16 pathways were activated,only 4 pathways were inhibited,and 5 pathways were not significantly changed.The glutamatergic synapse and GABAergic synapse were activated,while the serotonergic synapse was inhibited.Conclusions The symptoms of SHR include impatience and irritability,peripheral vascular dilation and collateral circulation formation,bulbar conjunctival congestive swelling,red tongue coloration,a dry tongue,constipation,red-yellow urine of low volume,and a rapid heart rate and high respiratory rate.All these suggest that SHR is a syndrome of hypertension with hyperactivity of liver-yang.The material basis of SHR is not only related to lipid,amino acid,and carbohydrate metabolism disorders,but also may be related to metabolic disorders of glutaminergic,GABAergic,and serotonergic neural pathways.

Objective To evaluate the application value of the MR three-dimensional double inversion recovery(3D DIR)sequence in the diagnosis of optic neuritis(ON).Methods A retrospective analysis was conducted on MRI images from 40 patients with sus-pected ON.All patients underwent conventional T2 WI fat suppression(FS)and 3D DIR sequences.The lesion detection rate and diag-nostic accuracy of the intraorbital,intracanalicular,and intracranial segments of the optic nerve were compared between the two sequences,respectively.The receiver operating characteristic(ROC)curves were used to assess the diagnostic performance,and the intraclass correlation coefficient(ICC)were used to analyze interobserver consistency.Imaging assessments were independently performed by two senior and two junior radiologists.Results The sensitivity(SEN),specificity(SPE),and accuracy(ACC)in lesion detection of 3D DIR sequence were significantly better than those of conventional T2 WI FS sequence[odds ratio(OR)221 vs 104,P＜0.001].Notably,3D DIR sequence exhibited superior performance in detecting lesions in the intraorbital segment[area under the curve(AUC)0.915,OR=102]and intracanalicular segment(AUC 0.858,OR=51)compared with conventional T2WI FS sequence.Additionally,3D DIR sequence significantly improved diagnostic consistency among junior radiologists(ICC value increased from 0.469 to 0.655),bring-ing their diagnostic performance closer to that of senior radiologists(AUC improved to 0.883,ACC reached 90.1％).Conclusion The 3D DIR sequence has outstanding diagnostic efficacy in detecting ON lesions,significantly improving ACC and interobserver consistency,thereby offering strong support for the precise diagnosis of ON.

High altitude heart disease(HAHD)is a chronic mountain sickness in which the body is exposed to high altitude(＞2 500 m)hypobaric hypoxia environment for a long time.HAHD has high morbidity and poor prognosis,and pulmonary hypertension is the main causative mechanism for its develop-ment.The phosphodiesterase-5 inhibitor sildenafil has become a hot drug for the treatment of pulmonary hypertension.This paper reviews the progress of HAHD and discusses the mechanism of action and effectiveness of sildenafil in the treatment of HAHD,with a view to providing a basis for the treatment of HAHD with sildenafil.

ObjectiveTo establish a rat model of osteoarthritis and study the anti-inflammatory effects and mechanisms of fraxetin. MethodsEighteen 8-week-old male SPF-grade SD rats were randomly divided into three groups: Rats in the blank group received a right articular cavity injection of 50 μL of normal saline for 1 week; the model and intervention groups were injected with monosodium iodoacetate (MIA) into the right joint cavity to induce osteoarthritis, while the intervention group subsequently received fraxetin (5 mg·kg^-1·d^-1) for 1 week. Four weeks after drug intervention, abdominal aortic blood was collected. The animals were then euthanized, and knee joint cartilage were collected. The cartilage samples were stained with hematoxylin-eosin, safranin O-fast green, and toluidine blue for histopathological examination and scoring using the Mankin and OARSI scoring systems. The trabecular bone volume/total volume (Tb.BV/TV), trabecular bone surface density/total volume (Tb.BS/TV), and trabecular number (Tb.N) of each group were compared and analyzed using a micro-CT scanning system. The expression levels of various inflammatory factors [tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6)], and cartilage oligomeric matrix protein (COMP) were measured using enzyme-linked immunosorbent assay (ELISA). The expression levels of mitogen-activated protein kinase p38 (p38 MAPK), phosphorylation-p38 MAPK (p-p38 MAPK), c-Jun N-terminal kinase (JNK), and phosphorylation-JNK (p-JNK) were measured by western blotting. ResultsThe staining of cartilage sections of rat knee joints showed that the articular surface defects in the model group were severe, while the cartilage destruction in the intervention group was relatively reduced. Micro-CT results showed that Tb.BV/TV, Tb.BS/TV and Tb.N in the intervention group were significantly higher than those in the model group (P < 0.05); the Mankin score in the model group was significantly higher than that in the blank group (P < 0.05), the Mankin score in the intervention group was significantly lower than that in the model group (P < 0.05); while the OARSI score in the intervention group was significantly lower than that in the model group (P < 0.05). The results of the enzyme-linked immunosorbent assay showed that the serum levels of TNF-α, IL-1β, IL-6, and COMP in the model group were significantly higher than those in the blank group (all P < 0.05), while those in the intervention group were significantly lower than in the model group (P < 0.05). Western blot results showed that the expression levels of p-p38 MAPK and p-JNK in the knee cartilage tissue were significantly lower in the intervention group than in the model group (both P < 0.05), and significantly higher in the model group than in the blank group (both P < 0.05). ConclusionFraxetin may play a therapeutic role in a monosodium iodoacetate-induced rat model of osteoarthritis through the p38 MAPK pathway.

ObjectiveTo establish a rat model of osteoarthritis and study the anti-inflammatory effects and mechanisms of fraxetin. MethodsEighteen 8-week-old male SPF-grade SD rats were randomly divided into three groups: Rats in the blank group received a right articular cavity injection of 50 μL of normal saline for 1 week; the model and intervention groups were injected with monosodium iodoacetate (MIA) into the right joint cavity to induce osteoarthritis, while the intervention group subsequently received fraxetin (5 mg·kg^-1·d^-1) for 1 week. Four weeks after drug intervention, abdominal aortic blood was collected. The animals were then euthanized, and knee joint cartilage were collected. The cartilage samples were stained with hematoxylin-eosin, safranin O-fast green, and toluidine blue for histopathological examination and scoring using the Mankin and OARSI scoring systems. The trabecular bone volume/total volume (Tb.BV/TV), trabecular bone surface density/total volume (Tb.BS/TV), and trabecular number (Tb.N) of each group were compared and analyzed using a micro-CT scanning system. The expression levels of various inflammatory factors [tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6)], and cartilage oligomeric matrix protein (COMP) were measured using enzyme-linked immunosorbent assay (ELISA). The expression levels of mitogen-activated protein kinase p38 (p38 MAPK), phosphorylation-p38 MAPK (p-p38 MAPK), c-Jun N-terminal kinase (JNK), and phosphorylation-JNK (p-JNK) were measured by western blotting. ResultsThe staining of cartilage sections of rat knee joints showed that the articular surface defects in the model group were severe, while the cartilage destruction in the intervention group was relatively reduced. Micro-CT results showed that Tb.BV/TV, Tb.BS/TV and Tb.N in the intervention group were significantly higher than those in the model group (P < 0.05); the Mankin score in the model group was significantly higher than that in the blank group (P < 0.05), the Mankin score in the intervention group was significantly lower than that in the model group (P < 0.05); while the OARSI score in the intervention group was significantly lower than that in the model group (P < 0.05). The results of the enzyme-linked immunosorbent assay showed that the serum levels of TNF-α, IL-1β, IL-6, and COMP in the model group were significantly higher than those in the blank group (all P < 0.05), while those in the intervention group were significantly lower than in the model group (P < 0.05). Western blot results showed that the expression levels of p-p38 MAPK and p-JNK in the knee cartilage tissue were significantly lower in the intervention group than in the model group (both P < 0.05), and significantly higher in the model group than in the blank group (both P < 0.05). ConclusionFraxetin may play a therapeutic role in a monosodium iodoacetate-induced rat model of osteoarthritis through the p38 MAPK pathway.