Aging-Us最新文献

筛选
英文 中文
Association of frailty and chronic limb-threatening ischemia in patients on maintenance hemodialysis: a prospective cohort study. 维持性血液透析患者虚弱和慢性肢体威胁缺血的关联:一项前瞻性队列研究。
IF 3.9 3区 医学
Aging-Us Pub Date : 2024-12-31 DOI: 10.18632/aging.206178
Mu-Yang Hsieh, Chien-Ming Luo, Chi-Hong Cheng, Li-Pei Dai, Chiu-Hui Chen, Shao-Yuan Chuang, Chung-Wei Yang, Chih-Cheng Wu
{"title":"Association of frailty and chronic limb-threatening ischemia in patients on maintenance hemodialysis: a prospective cohort study.","authors":"Mu-Yang Hsieh, Chien-Ming Luo, Chi-Hong Cheng, Li-Pei Dai, Chiu-Hui Chen, Shao-Yuan Chuang, Chung-Wei Yang, Chih-Cheng Wu","doi":"10.18632/aging.206178","DOIUrl":"10.18632/aging.206178","url":null,"abstract":"<p><p>Chronic limb-threatening ischemia (CLTI) is a prevalent yet unpredictable complication among patients undergoing hemodialysis, and frailty is linked to adverse outcomes in this population. This study examined the influence of clinical factors on vascular events in patients undergoing hemodialysis. This multicenter prospective cohort study included patients undergoing maintenance hemodialysis since January 2008. The initial cohort consisted of 1,136 patients, 828 of whom successfully underwent a frailty test. CLTI events were recorded at 3-month intervals until December 31, 2022. The mean patient age was 67 years, and 48% were female. Overall, 34% of participants were frail, 38% pre-frail, and 28% not frail. Frailty phenotype was associated with age, female sex, low educational level, diabetes mellitus, and history of stroke. During a median follow-up of 1461 days, 104 patients experienced CLTI events (not frail, 6.5%; pre-frail, 11%; frail, 20%; <i>P</i> < 0.001). Frail patients had a higher risk of CLTI than those who were non-frail (hazard ratio (HR) 3.94; 95% confidence interval (CI) 2.22-6.99; <i>P</i> < 0.001). After multivariable adjustment for age and comorbidities, frailty remained significantly associated with CLTI (HR 3.26; 95% CI 1.76-5.85; <i>P</i> < 0.001). Conclusively, these findings highlight the risk of CLTI in frail patients undergoing hemodialysis.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"null ","pages":"13676-13692"},"PeriodicalIF":3.9,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11723663/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142904118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Correction for: PTPRD mutation is a prognostic biomarker for sensitivity to ICIs treatment in advanced non-small cell lung cancer. 更正PTPRD突变是晚期非小细胞肺癌对ICIs治疗敏感性的预后生物标志物。
IF 3.9 3区 医学
Aging-Us Pub Date : 2024-12-31 DOI: 10.18632/aging.206186
Zhixuan Ren, Li Wang, Chaohui Leng
{"title":"Correction for: PTPRD mutation is a prognostic biomarker for sensitivity to ICIs treatment in advanced non-small cell lung cancer.","authors":"Zhixuan Ren, Li Wang, Chaohui Leng","doi":"10.18632/aging.206186","DOIUrl":"10.18632/aging.206186","url":null,"abstract":"","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"16 22","pages":"13693"},"PeriodicalIF":3.9,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11723662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142933659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Cell-type specific epigenetic clocks to quantify biological age at cell-type resolution. 以细胞类型分辨率量化生物年龄的细胞类型特异性表观遗传时钟。
IF 3.9 3区 医学
Aging-Us Pub Date : 2024-12-29 DOI: 10.18632/aging.206184
Huige Tong, Xiaolong Guo, Macsue Jacques, Qi Luo, Nir Eynon, Andrew E Teschendorff
{"title":"Cell-type specific epigenetic clocks to quantify biological age at cell-type resolution.","authors":"Huige Tong, Xiaolong Guo, Macsue Jacques, Qi Luo, Nir Eynon, Andrew E Teschendorff","doi":"10.18632/aging.206184","DOIUrl":"10.18632/aging.206184","url":null,"abstract":"<p><p>The ability to accurately quantify biological age could help monitor and control healthy aging. Epigenetic clocks have emerged as promising tools for estimating biological age, yet they have been developed from heterogeneous bulk tissues, and are thus composites of two aging processes, one reflecting the change of cell-type composition with age and another reflecting the aging of individual cell-types. There is thus a need to dissect and quantify these two components of epigenetic clocks, and to develop epigenetic clocks that can yield biological age estimates at cell-type resolution. Here we demonstrate that in blood and brain, approximately 39% and 12% of an epigenetic clock's accuracy is driven by underlying shifts in lymphocyte and neuronal subsets, respectively. Using brain and liver tissue as prototypes, we build and validate neuron and hepatocyte specific DNA methylation clocks, and demonstrate that these cell-type specific clocks yield improved estimates of chronological age in the corresponding cell and tissue-types. We find that neuron and glia specific clocks display biological age acceleration in Alzheimer's Disease with the effect being strongest for glia in the temporal lobe. Moreover, CpGs from these clocks display a small but significant overlap with the causal DamAge-clock, mapping to key genes implicated in neurodegeneration. The hepatocyte clock is found accelerated in liver under various pathological conditions. In contrast, non-cell-type specific clocks do not display biological age-acceleration, or only do so marginally. In summary, this work highlights the importance of dissecting epigenetic clocks and quantifying biological age at cell-type resolution.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"16 22","pages":"13452-13504"},"PeriodicalIF":3.9,"publicationDate":"2024-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11723652/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142933658","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Impaired renal transporter gene expression and uremic toxin excretion as aging hallmarks in cats with naturally occurring chronic kidney disease. 肾脏转运蛋白基因表达受损和尿毒症毒素排泄作为自然发生的慢性肾病猫的衰老标志。
IF 3.9 3区 医学
Aging-Us Pub Date : 2024-12-20 DOI: 10.18632/aging.206176
Qinghong Li, James A Holzwarth, Bethany Smith, Sonia Karaz, Mathieu Membrez, Vincenzo Sorrentino, Stacie Summers, Julie Spears, Eugenia Migliavacca
{"title":"Impaired renal transporter gene expression and uremic toxin excretion as aging hallmarks in cats with naturally occurring chronic kidney disease.","authors":"Qinghong Li, James A Holzwarth, Bethany Smith, Sonia Karaz, Mathieu Membrez, Vincenzo Sorrentino, Stacie Summers, Julie Spears, Eugenia Migliavacca","doi":"10.18632/aging.206176","DOIUrl":"10.18632/aging.206176","url":null,"abstract":"<p><p>Aging leads to nephron senescence and chronic kidney disease (CKD). In cats, indoxyl sulfate (IxS) has been previously quantified and associated with CKD, and little is known about tubular transporters. Two cohorts of cats aged 6 to 21 years were enrolled. Cohort 1 included 41 colony cats with 28 control and 13 CKD cats. Cohort 2 had 30 privately-owned cats with 10 control and 20 CKD cats. In cohort 1, serum concentrations of IxS, trimethylamine N-oxide (TMAO), <i>p</i>-cresol sulfate (PCS), and phenyl sulfate were higher in CKD vs. control cats (all P<0.05). This observation was independently validated in cohort 2. Renal cortical and medullar tissues were collected from a third cohort of cats euthanized for humane reasons unrelated to the study. We provided the evidence that renal tubular transporter genes, OAT1, OAT4, OATP4C1, and ABCC2, but not OAT3, were expressed in the kidneys of cats, and their expressions were downregulated in CKD (all FDR<0.1). Cats and humans share 90.9%, 77.8%, and 82.5% identities in OAT1, OATP4C1, and ABCC2 proteins, respectively. In healthy cats, circulating TMAO and IxS are significantly correlated with age. Our study reveals impaired uremic toxin secretion and tubular transporter expression in cats with CKD.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"16 ","pages":"13588-13607"},"PeriodicalIF":3.9,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11723653/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142900624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Brown adipose tissue enhances exercise performance and healthful longevity. 褐色脂肪组织提高运动表现和健康长寿。
IF 3.9 3区 医学
Aging-Us Pub Date : 2024-12-18 DOI: 10.18632/aging.206179
Dorothy E Vatner, Jie Zhang, Stephen F Vatner
{"title":"Brown adipose tissue enhances exercise performance and healthful longevity.","authors":"Dorothy E Vatner, Jie Zhang, Stephen F Vatner","doi":"10.18632/aging.206179","DOIUrl":"10.18632/aging.206179","url":null,"abstract":"<p><p>Brown adipose tissue (BAT), a major subtypes of adipose tissues, is known for thermogenesis and promoting healthful longevity. Our hypothesis is that BAT protects against impaired healthful longevity, i.e., obesity, diabetes, cardiovascular disorders, cancer, Alzheimer's disease, and reduced exercise tolerance. While most prior studies have shown that exercise regulates BAT activation and improves BAT density, relatively few have shown that BAT increases exercise performance. In contrast, our recent studies with the regulator of G protein signaling 14 (RGS14) knockout (KO) model of extended longevity showed that it enhances exercise performance, mediated by its more potent BAT, compared with BAT from wild type mice. For example, when the BAT from RGS14 KO mice is transplanted to WT mice, their exercise capacity is enhanced at 3 days after BAT transplantation, whereas BAT transplantation from WT to WT mice increased exercise performance, but only at 8 weeks after transplantation. The goal of this research perspective is to review the role of BAT in mediating healthful longevity, specifically exercise capacity. In view of the ability of BAT to mediate healthful longevity and enhance exercise performance, it is likely that a pharmaceutical analog of BAT will become a novel therapeutic modality.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"undefined ","pages":"13442-13451"},"PeriodicalIF":3.9,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11723650/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142856203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Arginase-II gene deficiency reduces skeletal muscle aging in mice. 精氨酸酶ii基因缺乏可减少小鼠骨骼肌衰老。
IF 3.9 3区 医学
Aging-Us Pub Date : 2024-12-12 DOI: 10.18632/aging.206173
Matteo Caretti, Duilio Michele Potenza, Guillaume Ajalbert, Urs Albrecht, Xiu-Fen Ming, Andrea Brenna, Zhihong Yang
{"title":"Arginase-II gene deficiency reduces skeletal muscle aging in mice.","authors":"Matteo Caretti, Duilio Michele Potenza, Guillaume Ajalbert, Urs Albrecht, Xiu-Fen Ming, Andrea Brenna, Zhihong Yang","doi":"10.18632/aging.206173","DOIUrl":"10.18632/aging.206173","url":null,"abstract":"<p><p>Age-associated sarcopenia decreases mobility and is promoted by cell senescence, inflammation, and fibrosis. The mitochondrial enzyme arginase-II (Arg-II) plays a causal role in aging and age-associated diseases. Therefore, we aim to explore the role of Arg-II in age-associated decline of physical activity and skeletal muscle aging in a mouse model. Young (4-6 months) and old (20-24 months) wild-type (<i>wt</i>) mice and mice deficient in <i>arg-ii</i> (<i>arg-ii<sup>-/-</sup></i>) of both sexes are investigated. We demonstrate a decreased physical performance of old <i>wt</i> mice, which is partially prevented in <i>arg-ii<sup>-/-</sup></i> animals, particularly in males. The improved phenotype of <i>arg-ii<sup>-/-</sup></i> mice in aging is associated with reduced sarcopenia, cellular senescence, inflammation, and fibrosis, whereas age-associated decline of microvascular endothelial cell density, satellite cell numbers, and muscle fiber types in skeletal muscle is prevented in <i>arg-ii<sup>-/-</sup></i> mice. Finally, we demonstrate an increased <i>arg-ii</i> gene expression level in aging skeletal muscle and found Arg-II protein expression in endothelial cells and fibroblasts, but not in skeletal muscle fibers, macrophages, and satellite cells. Our results suggest that increased Arg-II in non-skeletal muscle cells promotes age-associated sarcopenia, particularly in male mice.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"null ","pages":"13563-13587"},"PeriodicalIF":3.9,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11723659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142820317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
ISarcoPRM algorithm for global operationalization of sarcopenia diagnosis. 肌少症诊断全局操作化的ISarcoPRM算法。
IF 3.9 3区 医学
Aging-Us Pub Date : 2024-12-11 DOI: 10.18632/aging.206174
Pelin Analay, Murat Kara, Levent Özçakar
{"title":"ISarcoPRM algorithm for global operationalization of sarcopenia diagnosis.","authors":"Pelin Analay, Murat Kara, Levent Özçakar","doi":"10.18632/aging.206174","DOIUrl":"10.18632/aging.206174","url":null,"abstract":"","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"16 ","pages":"13434-13435"},"PeriodicalIF":3.9,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11723657/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142815184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Gender-specification lifestyle factors associated with mild cognitive impairment among young-old adults in Taiwan. 台湾中青年轻度认知障碍之性别生活型态因素。
IF 3.9 3区 医学
Aging-Us Pub Date : 2024-12-10 DOI: 10.18632/aging.206172
Su-Wen Chuang, Ching-Wen Chen, Meng-Chang Lee, Yu-Hsuan Chen, Wen Su, Cheng-Jung Chen, Wei-Teing Chen, Po-Jen Hsiao, Chih-Chien Chiu, Sui-Lung Su
{"title":"Gender-specification lifestyle factors associated with mild cognitive impairment among young-old adults in Taiwan.","authors":"Su-Wen Chuang, Ching-Wen Chen, Meng-Chang Lee, Yu-Hsuan Chen, Wen Su, Cheng-Jung Chen, Wei-Teing Chen, Po-Jen Hsiao, Chih-Chien Chiu, Sui-Lung Su","doi":"10.18632/aging.206172","DOIUrl":"10.18632/aging.206172","url":null,"abstract":"<p><strong>Background: </strong>The prevalence of mild cognitive impairment (MCI) exhibits a positive correlation with age, particularly evident in the old-old female population. Lifestyle factors have been identified as crucial risk determinants for MCI. However, there is a scarcity of research focusing on lifestyle factors among young-old population.</p><p><strong>Objective: </strong>This study aimed to explore the lifestyle factors associated with MCI in young-old male and female.</p><p><strong>Methods: </strong>This study employed a cross-sectional design and utilized demographic and lifestyle data obtained from participants enrolled in the Taiwan Biobank (TWB) between 2008 and 2021, with 32,897 individuals aged 60 to 70 years old. Cognitive function was assessed using the Mini-Mental State Examination (MMSE), with a total score ranging from 0 to 30 points. The cut-off of MCI scores was ≤18, ≤21, and ≤25 according to the education level, respectively. Logistic regression analysis was employed to assess the association between lifestyles and cognitive function.</p><p><strong>Results: </strong>3,878 individuals (11.78%) suffered from MCI. Upon gender stratification, high exercise metabolic equivalents in male (OR = 0.8, 95% CI: 0.70 - 0.92) and moderate exercise in female serve as protective factors for MCI (OR = 0.78, 95% CI: 0.70 - 0.87). Additionally, diversified dietary preferences among female (OR = 0.80, 95% CI: 0.66 - 0.97) also emerge as protective factors for cognitive function.</p><p><strong>Conclusions: </strong>It is worth noting that male is advised to target a higher exercise metabolic equivalent, while female can attain cognitive benefits with moderate exercise and diversified dietary.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"16 ","pages":"13662-13675"},"PeriodicalIF":3.9,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11723654/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142808702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Nuclear lipid droplets: a novel regulator of nuclear homeostasis and ageing. 核脂滴:核稳态和衰老的新调节器。
IF 3.9 3区 医学
Aging-Us Pub Date : 2024-12-09 DOI: 10.18632/aging.206175
Konstantinos Palikaras, Nektarios Tavernarakis
{"title":"Nuclear lipid droplets: a novel regulator of nuclear homeostasis and ageing.","authors":"Konstantinos Palikaras, Nektarios Tavernarakis","doi":"10.18632/aging.206175","DOIUrl":"10.18632/aging.206175","url":null,"abstract":"<p><p>Aging is a fundamental driver of numerous life-threatening diseases, significantly compromising cellular structures and functions, including the integrity of the nucleus. A consistent feature of aging across diverse species is the progressive accumulation of lipid droplets (nLDs) within the nuclear compartment, which disrupts nuclear architecture and functionality. Notably, aging is accompanied by a marked increase in nLD accumulation at the nuclear envelope. Interventions known to extend lifespan, such as caloric restriction and reduced insulin signaling, significantly reduce both the rate of accumulation and the size of nLDs. The triglyceride lipase ATGL-1, which localizes to the nuclear envelope, plays a critical role in limiting nLD buildup and maintaining nuclear lipid balance, especially in long-lived mutant worms. These findings establish excessive nuclear lipid deposition as a key hallmark of aging, with profound implications for nuclear processes such as chromatin organization, DNA repair, and gene regulation. In addition, ATGL-1 emerges as a promising therapeutic target for preserving nuclear health, extending organismal healthspan, and combating age-related disorders driven by lipid dysregulation.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"undefined ","pages":"13436-13441"},"PeriodicalIF":3.9,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11723664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142803567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Therapeutic effects of Huangqi formula (Eefooton) in chronic kidney disease: clinical research and narrative literature review. 黄芪方治疗慢性肾脏病的临床研究及文献综述。
IF 3.9 3区 医学
Aging-Us Pub Date : 2024-12-07 DOI: 10.18632/aging.206170
Kuo-Cheng Lu, San-Chiang Wu, Tsuo-Cheng Lu, I-Shang Tzeng, Chun-En Kuo, Yu-Chiang Hung, Szu-Ying Wu, Te-Chuan Chen, Ming-Kai Tsai, Chih-Kuang Chuang, Wen-Long Hu
{"title":"Therapeutic effects of Huangqi formula (Eefooton) in chronic kidney disease: clinical research and narrative literature review.","authors":"Kuo-Cheng Lu, San-Chiang Wu, Tsuo-Cheng Lu, I-Shang Tzeng, Chun-En Kuo, Yu-Chiang Hung, Szu-Ying Wu, Te-Chuan Chen, Ming-Kai Tsai, Chih-Kuang Chuang, Wen-Long Hu","doi":"10.18632/aging.206170","DOIUrl":"10.18632/aging.206170","url":null,"abstract":"<p><strong>Objective: </strong>The study aimed to assess the clinical effects of employing the Huangqi formula (Eefooton; EFT) for chronic kidney disease (CKD) treatment. A narrative literature review was undertaken to elucidate the specific ingredients of EFT and their potential impact on renal health.</p><p><strong>Methods: </strong>A retrospective observational study investigated EFT treatment in outpatients with stable CKD (stages 3B to 5) from March 2019 to March 2021. Patients received 20 mL of EFT thrice daily for 6 months, along with standard treatment. Control groups were matched to the EFT cohort. Regular assessments of renal, liver functions, and lipid profiles were conducted.</p><p><strong>Results: </strong>Serum creatinine (Cr) and eGFR levels consistently improved in stage 3B CKD patients at each follow-up visit. At 6 months, improvement in Cr and eGFR was observed for stage 4 and 5 CKD. Stage 3B CKD patients exhibited notable reductions in systolic blood pressure after 3 and 6 months of EFT treatment. Remarkably, a substantial decrease in HbA1C was noted in stage 4 CKD individuals after three months of therapy. Additionally, stage 4 CKD patients saw a significant reduction in LDL levels after both 3 and 6 months of EFT treatment. A literature review on EFT ingredients indicated that the positive effects of EFT might be associated with its anti-inflammatory, antioxidant, and anti-fibrotic properties.</p><p><strong>Conclusions: </strong>This research demonstrated that incorporating EFT alongside standard treatment enhanced renal function in individuals with CKD. EFT is proposed as a feasible complementary treatment for CKD patients, emphasizing the importance of early intervention.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"16 ","pages":"13627-13647"},"PeriodicalIF":3.9,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11723655/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142803566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信