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        <title>Experimental Biology and Medicine | Aging section | New and Recent Articles</title>
        <link>https://www.ebm-journal.org/journals/experimental-biology-and-medicine/sections/aging</link>
        <description>RSS Feed for Aging section in the Experimental Biology and Medicine journal | New and Recent Articles</description>
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        <pubDate>2026-04-23T11:02:38.113+00:00</pubDate>
        <ttl>60</ttl>
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        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10796</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10796</link>
        <title><![CDATA[Enhanced oxidative stress resilience in C. elegans acox-1.1 mutants through CTL-3 and proteasomal regulation]]></title>
        <pubdate>2026-03-13T00:00:00Z</pubdate>
        <category>Brief Communication</category>
        <author>Woori Bae</author><author>Mina Norman</author><author>Myon Hee Lee</author>
        <description><![CDATA[Oxidative stress is a primary driver of aging, necessitating robust cellular adaptation mechanisms. While peroxisomal β-oxidation and proteasomal degradation are known to influence stress responses, their functional crosstalk remains elusive. In this study, we show that C. elegans acox-1.1 mutants, despite having a shortened lifespan under normal conditions, exhibit a paradoxical resistance to mild chronic oxidative stress (1 mM paraquat, PQ) compared to wild-type worms. This PQ-induced resistance in acox-1.1 mutants was independent of the canonical SKN-1 pathway but required the peroxisomal catalase CTL-3. RNA-mediated knockdown of ctl-3 largely abolished the stress resistance of acox-1.1 mutants, leading to rapid mortality. Proteomic and biochemical analyses revealed that acox-1.1 mutants possess reduced levels of PAS-5, a core 20S proteasome subunit, resulting in impaired proteasomal assembly and accumulation of ubiquitinated (Ub) substrates under basal conditions. Intriguingly, exposure to 1 mM PQ significantly reduced the Ub-smear in acox-1.1 mutants, suggesting a metabolic shift where the cell prioritizes ROS scavenging over ATP-dependent protein degradation. Under oxidative stress, acox-1.1 mutants bypass defective proteasomal machinery and redirect energy toward CTL-3-mediated antioxidant defense. This study identified a peroxisomal adaptation mechanism whereby reduced proteasome complexity, coupled with enhanced ROS-regulatory machinery, confers survival advantages under specific oxidative challenges.]]></description>
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        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10808</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10808</link>
        <title><![CDATA[Mapping microglial mechanisms in Alzheimer’s disease: a comprehensive analysis]]></title>
        <pubdate>2025-12-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xiaofang Wang</author><author>Yuqing Guo</author><author>Yonghan Zha</author><author>Shuling Wang</author><author>Weihua Yang</author><author>Qianfang Jia</author>
        <description><![CDATA[Microglia, the brain’s primary immune cells, play crucial roles in Alzheimer’s disease (AD) pathogenesis. However, existing research remains abundant yet fragmented. Therefore, this study aimed to systematically identify hotspots and trends in microglia-related AD research, while providing an in-depth analysis of the underlying mechanisms to advance mechanistic understanding and therapeutic development. To achieve this, articles on microglia in AD were retrieved from the Web of Science Core Collection (WoSCC) database, and bibliometric analysis was performed using the WoSCC platform and CiteSpace 6.3.R1, with a focus on global collaboration, institutional and journal contributions, keyword bursts, and high-impact articles to comprehensively elucidate the underlying mechanisms. In total, 1,043 articles from 67 countries and regions were included.Among them, the United States led with 484 articles and an H-index of 100, followed by China with 276 articles. The University of California system (77 articles) and Harvard University (74 articles) had the highest H-index, both at 41. Journal of Neuroinflammation published the most articles (57 articles). Burst keywords persisting until 2024 included “memory,” “NLRP3 inflammasome,” and “system.” High-impact studies emphasized microglial roles in AD pathology, including Aβ clearance, synaptic pruning, inflammation, metabolism, phenotype shifts, immune memory, and genetic variation. Overall, microglial mechanisms are at the forefront of AD research. The United States leads in both article number and influence, followed by China. The University of California system and Harvard University demonstrate the greatest output and impact. Journal of Neuroinflammation is the leading journal. Microglial NLRP3 activation, system-level interactions, and memory impairment have emerged as key research hotspots in AD. Future research will focus on microglial mechanisms and therapeutic targets in AD.]]></description>
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        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10149</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10149</link>
        <title><![CDATA[Corrigendum: Quercetin suppresses ovariectomy-induced osteoporosis in rat mandibles by regulating autophagy and the NLRP3 pathway]]></title>
        <pubdate>2024-05-17T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Yue Xiong</author><author>Cheng-Wei Huang</author><author>Chao Shi</author><author>Liang Peng</author><author>Yu-Ting Cheng</author><author>Wei Hong</author><author>Jian Liao</author>
        <description></description>
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        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10117</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10117</link>
        <title><![CDATA[Age-related changes after intracerebral hemorrhage: a comparative proteomics analysis of perihematomal tissue]]></title>
        <pubdate>2024-03-25T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xinhui Li</author><author>Zhongsong Xiao</author><author>Peizheng Li</author><author>Wensong Yang</author><author>Yiqing Shen</author><author>Fangyu Liu</author><author>Xin Xiong</author><author>Qingyuan Wu</author><author>Peng Wang</author><author>Ruozhi Dang</author><author>Siwen Gui</author><author>Lan Deng</author><author>Anatol Manaenko</author><author>Peng Xie</author><author>Qi Li</author>
        <description><![CDATA[The risk factors and causes of intracerebral hemorrhage (ICH) and the degree of functional recovery after ICH are distinct between young and elderly patients. The increasing incidence of ICH in young adults has become a concern; however, research on the molecules and pathways involved ICH in subjects of different ages is lacking. In this study, tandem mass tag (TMT)-based proteomics was utilized to examine the protein expression profiles of perihematomal tissue from young and aged mice 24 h after collagenase-induced ICH. Among the 5,129 quantified proteins, ICH induced 108 and 143 differentially expressed proteins (DEPs) in young and aged mice, respectively; specifically, there were 54 common DEPs, 54 unique DEPs in young mice and 89 unique DEPs in aged mice. In contrast, aging altered the expression of 58 proteins in the brain, resulting in 39 upregulated DEPs and 19 downregulated DEPs. Bioinformatics analysis indicated that ICH activated different proteins in complement pathways, coagulation cascades, the acute phase response, and the iron homeostasis signaling pathway in mice of both age groups. Protein–protein interaction (PPI) analysis and ingenuity pathway analysis (IPA) demonstrated that the unique DEPs in the young and aged mice were related to lipid metabolism and carbohydrate metabolism, respectively. Deeper paired-comparison analysis demonstrated that apolipoprotein M exhibited the most significant change in expression as a result of both aging and ICH. These results help illustrate age-related protein expression changes in the acute phase of ICH.]]></description>
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