Biogerontology最新文献

{"title":"The role of tendon and ligament vasculature in ageing and injury.","authors":"Nodoka Iwasaki, Elizabeth J T Finding, Caroline P D Wheeler-Jones, Chavaunne T Thorpe","doi":"10.1007/s10522-026-10491-4","DOIUrl":"https://doi.org/10.1007/s10522-026-10491-4","url":null,"abstract":"<p><p>Ageing is a fundamental biological process marked by declining physiological function and the accumulation of stress-induced damage. It contributes to chronic disease and drives widespread alterations across organ systems, including the vasculature. Ageing of the macro- and microvasculature impairs nutrient delivery, promotes tissue degeneration, and reduces repair capacity in many tissues, including those of the musculoskeletal system. Tendons and ligaments become increasingly injury-prone with age, yet the relationship between vascular ageing and tendon and ligament in health and disease remains insufficiently understood. This review critically examines the effects of vascular ageing on tendons and ligaments, including their interfaces with muscle and bone. Emerging evidence indicates that age-related vascular decline contributes to structural and functional impairments in these tissues, accelerating musculoskeletal deterioration. We also discuss therapeutic approaches targeting vascular dysfunction, including growth factor modulation through use of platelet-rich plasma, gene-based strategies, and stem cell therapies, which show potential for mitigating age-related deficits. By synthesizing existing knowledge, this review emphasizes the need for further research into vascular ageing and its implications for tendon and ligament health. A deeper understanding of these processes could inform the development of innovative therapies aimed at preserving vascular function and improving quality of life in the ageing population.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 5","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13493437/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148787968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"When is health adequate for older adults? Optimal standards, patient-defined thresholds, and the weight of inequality.","authors":"Daniel Hernández-Pando","doi":"10.1007/s10522-026-10492-3","DOIUrl":"https://doi.org/10.1007/s10522-026-10492-3","url":null,"abstract":"<p><p>This perspective distinguishes two standards that are often used as if they were interchangeable. Optimal health is a standard built by medicine and expressed through guideline targets and biomarkers. Adequate health is the threshold of functioning that allows a person to live in a way they themselves experience as sufficient and dignified. Building on the concept of homeodynamic space as the biological substrate of adequate independence, on the older salutogenic tradition that asked what sustains health rather than only what causes disease, and on clinical evidence that aligning care with patients' own priorities can reduce treatment burden without worsening the outcomes patients themselves value, this article argues that optimal health is doctor based while adequate health is patient based. In any population ageing under conditions of socioeconomic inequality and health system fragmentation, the distance between the two standards is wide and unevenly distributed within the same country. Adequate health for an older adult must therefore be defined relative to the resources, culture, attitude, and priorities actually available to that person, not only against a uniform biomedical ideal that a large share of any population has no realistic path to reach. The argument is developed using data and policy from Mexico, chosen for the scale of its ageing population and the sharpness of its socioeconomic gradient, but the distinction it defends applies wherever health systems and biomarkers are used to judge the value of an older life.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 5","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13490212/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148787959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age-dependent physiological responses and longevity in three Drosophila species with contrasting lifespans exposed to low temperature and constant darkness.","authors":"Mikhail V Shaposhnikov, Liubov A Koval, Nadezhda V Zemskaya, Eugenia V Schegoleva, Tatyana V Babak, Ekaterina N Proshkina, Denis A Golubev, Natalya R Pakshina, Natalia S Timusheva, Elena Y Platonova, Anastasia A Gorbunova, Daria V Mikhailova, Alexey Moskalev","doi":"10.1007/s10522-026-10485-2","DOIUrl":"https://doi.org/10.1007/s10522-026-10485-2","url":null,"abstract":"<p><p>Aging is influenced by both genetic and environmental factors, yet comparative studies across species with different natural lifespans remain limited. We examined how reduced ambient temperature (18 °C vs 25 °C) and constant darkness, compared with a 12 h light/12 h dark cycle (DD vs LD), affect lifespan, age-related physiological traits, and gene expression in three Drosophila species with contrasting natural lifespans and climatic adaptations (tropical, short‑lived D. kikkawai, tropical, intermediate‑lived D. melanogaster, and temperate, long‑lived D. virilis). Low temperature extended lifespan in all three species, with the largest relative gains occurring in the shortest‑lived D. kikkawai males, yet the longest absolute lifespans were consistently attained by the long‑lived D. virilis. Constant darkness moderately increased lifespan at 25 °C, particularly in males, but its combination with low temperature became antagonistic in D. virilis, revealing that the interaction between photoperiod and temperature depends on both baseline longevity and sex. Longer lifespan correlated with lower metabolic rate, greater body mass, and sustained late‑life activity. Gene expression analyses in D. melanogaster revealed that low temperature induced a youthful metabolic and immune profile, whereas DD often counteracted these changes. Our findings do not support a simple inverse or direct relationship between baseline longevity and geroprotective efficacy. Instead, these results suggest that the responses to low temperature and darkness are species‑ and sex‑specific and reflect each species' evolutionary and ecological background.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 5","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Luteolin and glycitein from Codonopsis pilosula ameliorate age-related locomotor decline in C. elegans via DAF-16-dependent but autophagy-divergent pathways.","authors":"Yan Zhuang, Lulu Yi, Can Zhang, Lu Chen, Ajia Chen, Gong Tang, Zhiling Li, Zhongliang Hu","doi":"10.1007/s10522-026-10490-5","DOIUrl":"10.1007/s10522-026-10490-5","url":null,"abstract":"<p><p>As global population aging accelerates, maintaining locomotor function in later life has become a critical biomedical challenge. This study investigates the effects of three bioactive compounds-Luteolin (Lut), Glycitein (Gly), and α-Spinasterol (α-Spin)-isolated from the traditional Chinese medicinal herb Codonopsis pilosula (Dangshen), on age-related locomotor decline using the Caenorhabditis elegans (C.elegans) model. We demonstrate that Lut and Gly significantly ameliorate the deterioration of body bend and thrashing frequencies in aged nematodes. Further analysis reveals that both compounds mitigate age-associated sarcopenia by reducing abnormalities in muscle structure and mitochondrial morphology. Mechanistically, we found that the beneficial effects of Lut and Gly on locomotion are dependent on the transcription factor DAF-16/FOXO, as both compounds promote DAF-16 nuclear translocation and the effects are abolished upon daf-16 knockdown. However, these compounds diverge in their regulation of autophagy: Lut improves locomotion through an lgg-1-dependent autophagy-related process, whereas Gly exerts its effects independently of the autophagic pathway. In contrast, α-Spin, despite altering autophagosome levels, did not improve locomotor capacity. These findings elucidate the distinct pharmacological mechanisms of Codonopsis pilosula constituents, highlighting their potential as modulators of healthspan via DAF-16-dependent but mechanistically distinct pathways.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 4","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148720705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Isoorientin attenuates aging-induced bone deterioration by suppressing M1-mediated TLR4-MAPK-NF-κB inflammatory signaling.","authors":"Jinku Guo, Jun Xie, Ankai Xu, Wei Wang, Zhiqiang Fu, Kening Zhou, Shengkun Hong","doi":"10.1007/s10522-026-10488-z","DOIUrl":"10.1007/s10522-026-10488-z","url":null,"abstract":"<p><strong>Background: </strong>Aging disrupts bone remodeling by increasing osteoclast activity, reducing osteogenic capacity, and elevating inflammation. Toll-like receptor 4 (TLR4)-mediated inflammatory signaling has been implicated in bone degeneration, yet its role in age-related skeletal decline remains incompletely understood. Isoorientin, a plant-derived flavonoid with reported anti-inflammatory properties, has not been evaluated in the context of skeletal aging.</p><p><strong>Methods: </strong>Bone aging was first assessed in C57BL/6 J mice using micro-computed tomography (μCT), histology, TRAP staining, and immunofluorescence. The effects of isoorientin on osteogenesis were examined in senescent hBMSCs by alkaline phosphatase (ALP) activity, mineralization assays, and expression of osteogenesis-related genes. LPS-stimulated RAW264.7 cells were used to evaluate inflammatory responses and M1/M2 polarization. To assess TLR4/ mitogen-activated protein kinase (MAPK)/ nuclear factor-κB (NF-κB) regulation, RAW264.7 cells were treated with TAK-242 or TAK-242 plus isoorientin. Finally, aged mice were treated with isoorientin, TAK-242, or both to evaluate in vivo pathway modulation and bone protection.</p><p><strong>Results: </strong>Aged mice exhibited reduced trabecular mass, elevated osteoclast activity, and increased osteoclast-associated markers. Isoorientin treatment improved trabecular structure, decreased osteoclast numbers, and lowered osteoclast-associated proteins. In senescent hBMSCs, isoorientin restored ALP activity, enhanced mineral deposition, and increased osteogenic marker expression. Isoorientin also reduced pro-inflammatory cytokines, suppressed M1 polarization, and inhibited TLR4/MAPK/NF-κB activation. The combination of isoorientin and TAK-242 exhibited the most potent suppression of inflammatory signaling and the most significant enhancement in bone microarchitecture.</p><p><strong>Conclusion: </strong>Isoorientin alleviates age-related bone loss by suppressing TLR4-mediated inflammation, reducing osteoclast activation, and restoring impaired osteogenesis. These findings identify isoorientin as a promising therapeutic candidate for age-associated osteoporosis.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 4","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal biological ageing and telomere attrition across parity, pregnancy, and the postpartum period.","authors":"Laura Collopy, Yana Kolenichenko","doi":"10.1007/s10522-026-10487-0","DOIUrl":"10.1007/s10522-026-10487-0","url":null,"abstract":"<p><p>Telomere length (TL) is a well-established biomarker of biological ageing, sensitive to cumulative physiological and psychosocial stress. This review synthesises current evidence on how pregnancy, postpartum stressors, and reproductive history shape maternal biological ageing, integrating findings from telomere biology and emerging epigenetic ageing measures. Pregnancy represents a period of substantial metabolic, hormonal, and immunological demand and is increasingly conceptualised as a transient state of accelerated biological ageing. While telomere shortening is not consistently detectable during gestation, epigenetic clocks indicate a temporary increase in biological age, which is only partially reversible postpartum. Across the life course, higher parity is associated with shorter TL, with evidence suggesting a cumulative effect that becomes most apparent in later life and around the menopausal transition. However, this relationship is heterogeneous and modified by factors including age at last birth, breastfeeding, and socioeconomic context. Postpartum represents a critical and underexplored window in which sleep deprivation, psychological stress, and social factors converge to influence telomere dynamics. In particular, poor sleep quality and postpartum depression (PPD) are consistently linked to accelerated telomere attrition and epigenetic ageing, with emerging evidence of a bidirectional relationships whereby shorter TL may also predispose to PPD. Overall, evidence supports a model in which reproductive events impose are associated with measurable transient and cumulative costs to cellular ageing biomarkers. These findings highlight the importance of incorporating postpartum health, particularly sleep and mental health support, into life-course models of ageing and underscore the need for longitudinal, mechanistic, and intervention-focused research in maternal populations.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 4","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13457282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148700787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIRT1 in brain aging: molecular mechanisms and therapeutic potential of pharmacological and natural modulators.","authors":"Esraa M Mosalam, Mahmoud S Abdallah, Ahmed R Gardouh, Eman Hamza, Mostafa M Bahaa, Mahmoud Nazih, Reham A Al-Dhelaan, Noha Kamal","doi":"10.1007/s10522-026-10480-7","DOIUrl":"10.1007/s10522-026-10480-7","url":null,"abstract":"<p><p>Aging is a multifactorial process affects different tissues and organs and is modulated by genetic and environmental factors. In aging, the frequency of DNA repair errors and genomic instability are augmented. Depletion of endogenous antioxidant capacity during aging promotes the development of oxidative stress which triggers oxidative stress-induced DNA injury. Brain aging is manifested by cognitive impairment and memory disorders. Development of neuronal senescence is the major pathway in the progression of brain aging. Silent information regulator sirtuin 1 (SIRT1) is a class III histone deacetylase plays a critical role in genomic stability during aging. SIRT1 is highly expressed in specific brain regions involved in energy expenditure and metabolic activity that is necessary for brain development and control of brain senescence. Therefore, SIRT1 may have neuroprotective effects against brain aging and related neurodegenerative diseases. This narrative review aims to critically evaluate the role of SIRT1 in brain aging and to summarize current evidence on compounds that directly or indirectly modulate SIRT1 activity, with a focus on their mechanistic pathways and potential therapeutic implications. Findings of the present review highlighted that SIRT1 activators such as resveratrol, metformin and statins have neuroprotective effects against brain aging by regulating inflammatory and oxidative stress disorders through modulation of downstream signaling pathways.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 4","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic interactions between PIWI subfamily genes and hobo transposons modulate Drosophila melanogaster lifespan under chronic low-intensity irradiation.","authors":"Elena Yushkova","doi":"10.1007/s10522-026-10486-1","DOIUrl":"10.1007/s10522-026-10486-1","url":null,"abstract":"<p><p>In recent decades, there has been active research into how ionizing radiation at low doses, an inevitable factor in human activity, affects aging processes and which molecular genetic mechanisms underlie this influence. This study investigates the effects of mutations in PIWI subfamily genes (piwi and aub), which regulate transposable elements, on the lifespan of Drosophila melanogaster under conditions of genome instability induced by hobo transposons and chronic low-intensity irradiation (20 cGy). It is shown that dysfunction of piwi and aub modulates the activity of hobo transposons, increasing the frequency of their excisions/transpositions and recombinogenic activity, as confirmed by phenotypic and PCR analyses. The presence of hobo transposons in the genome elevates the spontaneous level of DNA fragmentation in ovarian cells, and chronic irradiation enhances this effect, leading to increased DNA damage in somatic and germline cells of most studied strains. Despite increased genetic instability and reduced fertility in some genotypes, the combined presence of mutations and hobo transposons paradoxically increases lifespan both under control conditions and after irradiation. Analysis of the interaction between genetic factors reveals a predominantly antagonistic, and in one case synergistic, effect on lifespan, depending on the type of mutation, the structure of the hobo transposons (full-size or defective copies), sex, and irradiation conditions. These results demonstrate the complex interplay between systems controlling transpositional activity and stress-induced processes that affect key viability parameters.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 4","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148676950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endurance training mitigates morphine-induced renal dysfunction in young and aged rats: involvement of oxidative stress, SIRT1, Klotho and TFAM.","authors":"Atena Alifarsangi, Saeedeh Ahmadinejad, Mohammad Amin Rajizadeh, Saeedeh Shojaeepour, Shahrzad Azizi, Alireza Keyhani, Fatemeh Darvishzadeh Mahani, Soheil Pardakhty","doi":"10.1007/s10522-026-10481-6","DOIUrl":"10.1007/s10522-026-10481-6","url":null,"abstract":"<p><strong>Background: </strong>Chronic morphine consumption induces oxidative stress and renal dysfunction, effects that may be exacerbated by aging-related declines in adaptive capacity. Regular endurance exercise enhances antioxidant defense and mitochondrial regulation; however, its ability to counteract morphine-induced renal alterations across different stages of aging remains insufficiently characterized.</p><p><strong>Methods: </strong>Male wistar rats, categorized as young and aged based on chronological age and body weight, were allocated to control, morphine, exercise, and morphine plus exercise groups within each age category. Morphine was administered via drinking water for four weeks. Concurrently, animals in the exercise groups performed moderate-intensity continuous training on a treadmill. At study completion, serum and renal tissues were collected for assessment of oxidative stress markers (MDA, TAC, SOD), MPO, renal function indices (BUN and creatinine), and renal expression of sirtuin 1 (SIRT1) and Klotho, Mitochondrial compatibility markers (Citrate synthase activity and TFAM).</p><p><strong>Results: </strong>Chronic morphine exposure was associated with increased oxidative stress markers and decreased antioxidant capacity in kidney tissue, and simultaneously increased serum urea and creatinine levels in young and old mice, indicating impaired renal functional status. Chronic morphine administration also decreased SIRT1 and Klotho levels in young and old animals. In contrast, 4 weeks of endurance training improved markers of mitochondrial adaptation, oxidative balance, and renal function, which were associated with increased expression of SIRT1 and Klotho in kidney tissue. These changes could indicate a potential link between exercise training and molecular pathways involved in the regulation of oxidative stress and renal homeostasis. However, these findings suggest an association, and causal or mechanistic interpretations will require further investigation in future studies.</p><p><strong>Conclusion: </strong>These findings indicate that endurance training is associated with more favorable renal biomarker profiles in the context of chronic opioid exposure.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 4","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148676974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research progress of traditional Chinese medicine interventions for aging-related nervous system diseases.","authors":"Xingyuan Du, Ziheng Shen, Yuanhao Xu, Weichu Song, Yanan Guo, Junping Kou, Shuaishuai Gong, Qianqian Ren","doi":"10.1007/s10522-026-10484-3","DOIUrl":"10.1007/s10522-026-10484-3","url":null,"abstract":"<p><p>Aging-related neurological disorders, including stroke, Alzheimer's disease (AD), Parkinson's disease (PD), epilepsy, and various neuroinflammatory conditions, affect over three billion individuals worldwide and constitute leading causes of morbidity, disability, and socioeconomic burdens. Aging contributes not only to the increased incidence of these disorders but also to their progression through interconnected mechanisms, including endothelial dysfunction, oxidative stress, chronic inflammation, mitochondrial dysfunction, cellular senescence, metabolic imbalance, and gut microbiota dysbiosis. These processes collectively impair neuronal survival, synaptic plasticity, and cognitive and motor functions. Traditional Chinese medicine (TCM), with its characteristic multi-component and multi-target therapeutic strategies, has emerged as a promising approach to counteract age-associated neurological decline. Accumulating preclinical studies suggest that TCM interventions may exert neuroprotective, anti-inflammatory, and antioxidant effects, modulate autophagy, restore metabolic homeostasis, and potentially delay cellular senescence. However, high-quality clinical evidence on safety and efficacy remains limited. This review summarizes current insights into the molecular interplay between aging and neurological disorders and highlights the therapeutic potential of TCM in targeting hallmarks of aging, providing perspectives for integrative prevention and treatment strategies for neurodegenerative and neurovascular diseases.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"27 4","pages":""},"PeriodicalIF":5.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148652872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}