AGEING RESEARCH REVIEWS衰老研究评论
AGEING RESEARCH REVIEWS(英文缩写 AGEING RES REV),ISSN 1568-1637,eISSN 1872-9649,中文译名:衰老研究评论 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 11.788 | Q1 |
| 2022 | 13.100 | Q1 |
| 2023 | 12.500 | Q1 |
| 2024 | 12.400 | Q1 |
| 2025 | 15.500 | Q1 |
AGEING RESEARCH REVIEWS 最新收录文献
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1. What can narcolepsy teach us about hypocretin and dementia?
1. 发作性睡病能教会我们什么关于下丘脑分泌素与痴呆症的知识？PMID:日期:2026-10-02Sleep and circadian disturbances are associated with cognitive decline and dementia. Narcolepsy type 1 (NT1), characterized by severe sleep-wake disruption and loss of hypocretin, would therefore be expected to predispose individuals to premature brain aging. Yet available biomarker and neuroimaging findings do not consistently support this possibility, raising questions about the role of hypocretin in mechanisms linking sleep to neurodegeneration. Beyond maintaining wakefulness, hypocretin interacts with inflammatory circuits, metabolic regulation, synaptic plasticity, amyloid processing, and circadian organization. Moreover, wake continuity and neuronal activity during this state may be relevant to the production and release of proteins implicated in neurodegeneration. The coexistence of profound sleep-wake abnormalities and an inconsistent neurodegenerative biomarker profile makes NT1 a unique human condition for investigating these relationships. Understanding this apparent paradox may provide new perspectives on how hypocretin, sleep-wake dynamics, neuronal signaling, and circadian biology relate to long-term brain health and dementia.
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2. Ferroptosis-Driven Inflammaging in Age-Associated Degenerative Disorders: Molecular Mechanisms and Therapeutic Potential of Natural Products.
2. 铁死亡驱动的年龄相关退行性疾病中的炎性衰老：天然产物的分子机制与治疗潜力PMID:日期:2026-10-01Persistent low-grade inflammation, oxidative stress, cellular senescence, and disturbance of cellular homeostasis are all connected with ageing and can lead to the development of age-related diseases. Ferroptosis, an iron-dependent type of controlled cell death, has been linked to these processes more and more. It may represent a key connection between inflammation, oxidative damage, and tissue failure as people age. With a focus on neurodegenerative, cardiovascular, metabolic, pulmonary, and musculoskeletal problems, this study explores the new idea of a ferroptosis-inflammaging axis and its role in age-associated degenerative disorders. The review addresses the data supporting ferroptosis as a potential therapeutic target and summarises the current understanding on the relationship between ferroptosis and the main biological processes linked to ageing. Natural products are given particular attention as possible ferroptosis modulators, emphasizing their therapeutic significance and the growing data from experimental models. Additionally included are the translational difficulties related to ferroptosis-targeted therapies, such as the lack of clinical validation, the development of biomarkers, pharmacokinetic issues, and disease-specific treatment approaches. All things considered, comprehending the ferroptosis-inflammaging axis may offer a foundation for discovering cutting-edge therapeutic strategies to delay tissue dysfunction and enhance healthy ageing.
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3. Redox-mitochondrial crosstalk in neurotoxicity: Regulated cell death pathways and neuroprotective strategies.
3. 神经毒性中的氧化还原-线粒体交互作用：调控性细胞死亡通路与神经保护策略PMID:日期:2026-09-30Neurotoxicity is an injury of the central or peripheral nervous system due to harmful stimuli including environmental chemicals, disease-associated endogenous stressors and other exposures that disturb neuronal homeostasis. A common outcome of neurotoxic stress is progressive disruption of synaptic function, redox balance and energy metabolism which together increase vulnerability to regulated cell-death programs. This review focuses on oxidative stress as core driver that shift reactive species from physiological signalling to direct chemical damage of lipids, proteins and DNA with mitochondria acting as a key integration point where oxidative damage and calcium dysregulation converge. We describe how mitochondrial dysfunction lowers the threshold for intrinsic apoptosis and how oxidative stress can also engage additional regulated death pathways relevant to neurotoxicity, including necroptosis, ferroptosis and parthanatos alongside endoplasmic reticulum stress and excitotoxicity that amplify the damage. Particular emphasis is placed on aging as a modifier of mitochondrial resilience and on the reciprocal interactions between disease-associated proteins, mitochondrial dysfunction and synaptic injury in major age-related neurodegenerative disorders. Finally, the review links these mechanisms to neurodegenerative diseases, acute neural injuries and environmental or chemical neurotoxins and summarizes neuroprotective strategies that target redox imbalance, mitochondrial stability and apoptosis-related signalling.
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4. Neuroenergetic Flexibility in the Aging Brain: Cellular Mechanisms and Diet-Induced Metabolic Switching.
4. 衰老大脑中的神经能量灵活性：细胞机制与饮食诱导的代谢转换PMID:日期:2026-09-26The aging brain undergoes progressive alterations in energy metabolism that may reduce its capacity to match energy supply with changing functional demands. Declining glucose metabolism, mitochondrial dysfunction, and altered neuron-glia and neurovascular interactions may contribute to this vulnerability, but these changes do not necessarily indicate complete loss of metabolic capacity. Neuroenergetic flexibility refers to the capacity to coordinate changes in substrate utilization with energetic demand while maintaining cellular and functional homeostasis. This review synthesizes evidence from cellular, animal, imaging, and clinical studies to examine the mechanisms underlying this capacity, how it changes with aging, and whether diet-induced metabolic switching can enhance it. Particular attention is given to the distinction between metabolic switching, defined as a change in the relative contribution of available substrates, and neuroenergetic flexibility, which requires coordinated adaptation across substrate delivery, cellular metabolism, mitochondrial processing, neurovascular support, and functional demand. Evidence indicates that ketogenic diets, intermittent fasting, and caloric restriction can alter substrate availability and utilization and can engage mitochondrial, cellular stress-response, and nutrient-sensing pathways. However, the strength of evidence differs across biological levels: changes in alternative-substrate utilization are more consistently demonstrated than coordinated improvements in mitochondrial, vascular, cellular, and functional outcomes. Thus, increased ketone utilization or other metabolic shifts should not, by themselves, be interpreted as evidence of restored neuroenergetic flexibility. Instead, the available evidence suggests that aging may preserve individual metabolic capacities while reducing the coordination and reserve required to adapt effectively to changing energetic demands. Dietary interventions therefore provide useful models for testing metabolic adaptability, but their ability to restore integrated neuroenergetic flexibility in aging or neurodegenerative disease remains uncertain and appears to depend on age, metabolic state, disease context, intervention characteristics, and adherence.
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5. Research Progress in Skin Anti-Aging Drugs Based on Core Pathological Drivers.
5. 基于核心病理驱动因素的皮肤抗衰老药物研究进展PMID:日期:2026-09-23Skin aging is driven by multiple interconnected pathological processes. However, existing evidence remains fragmented across studies of individual mechanisms and compounds, hindering the discovery of novel targets and the repurposing of established drug targets.This review systematically summarizes the fundamental mechanisms and categorizes current antiaging pharmacological strategies corresponding to these mechanisms, aiming to provide a theoretical framework for future drug development and clinical translation. PubMed/MEDLINE and ClinicalTrials.gov were searched from inception through June 2026 using core and compound-specific strategies. Eligible reports evaluated defined interventions for intrinsic skin aging or photoaging and reported efficacy, mechanistic, or safety outcomes. Of 7,973 records identified, 675 duplicates and 6,933 records were removed during AI-assisted prescreening, leaving 365 for human screening. The final synthesis included 91 reports covering 47 intervention classes. Data were extracted into nine prespecified fields, classified using a five-level evidence hierarchy, and synthesized narratively because heterogeneity precluded meta-analysis. Current evidence indicates that oxidative stress functions not only as an initiating trigger, but a parallel amplifier, and a downstream consequence within the bidirectional feedback loops of mitochondrial dysfunction and other aging mechanisms. It connects multiple aging-related pathways as a central hub. Interventions targeting oxidative stress have demonstrated promising outcomes in both in vitro and in vivo studies. Accordingly, we propose an evidence-stratified, mechanism-to-translation framework integrating skin organoid models, nanoparticle-based delivery systems, and artificial intelligence-driven target screening to guide multimechanism intervention strategies, facilitate targeted drug development, and accelerate precision clinical translation.
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6. Age-Related Metabolic Vulnerability of Glia in Intracerebral Hemorrhage: Mechanisms and Therapeutic Opportunities.
6. 脑出血中胶质细胞的年龄相关代谢脆弱性：机制与治疗机遇PMID:日期:2026-09-22Intracerebral hemorrhage (ICH), caused by the rupture of blood vessels within the brain parenchyma, represents the most severe form of stroke, characterized by the highest mortality rate and predominantly affecting the elderly population. Glial cells, including microglia, astrocytes, and oligodendrocytes, serve as the resident immune cells of the central nervous system and undergo significant metabolic reprogramming following ICH. Microglia exhibit dual roles in post-ICH tissue damage by altering their polarization states: they contribute to secondary brain injury through pro-inflammatory responses while also promoting hematoma clearance via anti-inflammatory mechanisms. Astrocytes primarily provide neuroprotective effects by extending branched processes to maintain neuronal architecture and preserve the integrity of the blood-brain barrier. Oligodendrocytes are susceptible to metabolic dysregulation following ICH, leading to myelin sheath damage and subsequent axonal dysfunction. Metabolically, the acute phase of ICH is marked by suppressed glucose metabolism, which gradually normalizes in later stages. Concurrently, oxidative stress and lipid peroxidation disrupt glial cell homeostasis. The extravasation of blood components leads to iron overload, exacerbating metabolic disturbances through impaired iron regulation. These metabolic disruptions propagate through intracellular signaling pathways, thereby influencing glial pathophysiology. Unlike previous reviews that primarily describe these changes, this review offers a conceptual framework that explicitly integrates aging, metabolic reprogramming, and intercellular communication across different phases of injury. We critically assess the robustness of current evidence, differentiate between correlative observations and causal mechanisms, and identify significant knowledge gaps. We conclude that the age-related metabolic vulnerability of glial cells constitutes a promising therapeutic target, and we propose testable hypotheses to guide future mechanistic and translational research. By synthesizing recent literature within this integrative framework, this review seeks to enhance understanding of metabolic regulation in glial cells following ICH, thereby laying the groundwork for the development of targeted metabolic interventions.
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7. Association between muscle fatigability, self-perceived fatigue and inflammation in older adults: A systematic literature review.
7. 老年人肌肉疲劳性、自感疲劳与炎症之间的关联：一项系统性文献综述PMID:日期:2026-09-22Muscle fatigability (MF) and self-perceived fatigue (SPF) are two intertwined dimensions of fatigue. Chronic inflammation is a hallmark of ageing and contributes to the pathophysiology fatigue. To review published literature on the association between circulating inflammatory biomarkers and both MF and SPF in older adults. PubMed, Web of Science, and PSycINFO were systematically screened for publications reporting on MF and/or SPF and inflammation in adults aged 65 and above, resulting in 7009 articles. Measures of the association between MF or SPF and systemic inflammation were extracted from the included studies. When possible, a meta-correlation was performed. 27 articles (4962 patients) were included in this study. Meta-correlations showed that IL-6 was significantly correlated with both MF (7 studies; r = -0.189, p = 0.0017) and SPF (2 studies; r = 0.160, p = 0.0241). TNF-α had no significant correlation with MF (4 studies; r = -0.052, p = 0.196) and data were insufficient to perform a meta correlation with SPF. CRP did not significantly correlate with MF (4 studies; r = -0.078, p = 0.19), while high heterogeneity precluded correlation with SPF. The studies not included in the meta-correlations confirmed the significant association between IL-6 and both MF (3 studies) and SPF (5 studies). These studies also showed a significant association between CRP and SPF (6 studies) and between TNF-α and both MF (1 study) and SPF (1 study). A significant correlation between fatigue (MF and SPF) and inflammation was found. Among the inflammatory biomarkers investigated, IL-6 showed the most consistent association with both MF and SPF across the included studies.
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8. Frailty-targeted cardiovascular rehabilitation and management in older adults with cardiovascular disease and frailty: a systematic review and meta-analysis.
8. 针对患有心血管疾病和衰弱的老年人的衰弱靶向心血管康复与管理：一项系统综述和荟萃分析PMID:日期:2026-09-22To evaluate the effectiveness and delivery characteristics of frailty-related cardiovascular rehabilitation and management interventions for older adults with cardiovascular disease and frailty. We systematically reviewed randomized controlled trials (RCTs) and non-randomized studies of interventions (NRSIs) identified through searches of PubMed, Embase, Web of Science, CINAHL via EBSCOhost, and the Cochrane Library from inception to 30 April 2026. Random-effects meta-analyses used conventional restricted maximum-likelihood estimation. Certainty of evidence was assessed using the GRADE framework. Sixteen studies (13 RCTs and 3 NRSIs; 1716 enrolled participants) were included. Significant effects favoured the intervention on adjusted/model-based Short Physical Performance Battery (SPPB) (MD 1.20 points, 95% CI 0.54-1.87; k = 2), 6-minute walk distance (MD 29.84 m, 95% CI 15.81-43.87; k = 2), frailty burden (Hedges'g [bias-corrected SMD] -1.94, 95% CI -2.99 to -0.88; k = 2), lower-limb strength (Hedges'g [bias-corrected SMD] 1.48, 95% CI 0.42-2.55; k = 2), and SPPB decline (RR 0.32, 95% CI 0.16-0.67; k = 3), but not on unadjusted SPPB, SPPB improvement, handgrip strength, Barthel scores, or all-cause mortality. Hospitalization and quality-of-life outcomes were not pooled for uncomparable definitions or constructs. Safety, implementation and economic evaluation were heterogeneously or even not reported. The certainty of evidence was rated as very low. The evidence suggests favourable but uncertain signals for selected proximal functional outcomes, with no clear benefit for distal clinical outcomes. These findings remain exploratory, and clinically meaningful benefit has not been established, given the limited evidence base, risk of bias, heterogeneity, imprecision, and very low certainty of evidence.
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9. Immunosenescence in Uveitis: From Mechanistic Insights to Therapeutic Implications.
9. 葡萄膜炎中的免疫衰老：从机制洞察到治疗意义PMID:日期:2026-09-22Immunosenescence-the age-associated remodeling of the immune system-has emerged as a potential modifier of chronic inflammatory disease. This review examines the evidence that immunosenescence may contribute to the chronicity, refractoriness, and therapeutic heterogeneity of uveitis, and considers the clinical and translational implications of this framework. It first outlines the features of immune aging, including thymic involution, contraction of the naïve T cell pool, accumulation of memory and terminally differentiated populations, and a chronic low-grade inflammatory state (inflammaging), and discusses signaling pathways that have been associated with these processes, including AMPK-mTOR, NF-κB, cGAS-STING, and JAK-STAT. It then evaluates three complementary but unequal lines of evidence relevant to uveitis: direct human observations from peripheral blood and intraocular fluids, mechanistic support from experimental models, and contextual inference from age-associated ocular disorders. Collectively, these data suggest that age-related immune remodeling may promote breakdown of ocular immune privilege, blood-retinal barrier dysfunction, persistent cytokine signaling, and incomplete response to conventional therapy in selected uveitis phenotypes. Finally, this review discusses therapeutic implications, including Treg enhancement, cytokine-directed approaches, and advanced drug delivery, while emphasizing that direct evidence of immune rejuvenation in human uveitis remains lacking. Ageing does not simply amplify ocular inflammation; it may attenuate selected acute immune responses while impairing resolution and tissue resilience, with effects that depend on disease context. By bridging geroscience and ocular immunology, this review offers a translational framework for understanding refractory intraocular inflammation and highlights future priorities for biomarker development, patient stratification, and precision medicine in uveitis.
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10. Nuclear medicine-based diagnosis and therapeutic strategies for neurodegenerative diseases: Clinical progress.
10. 基于核医学的神经退行性疾病诊断与治疗策略：临床进展PMID:日期:2026-09-21Neurodegenerative diseases (NDs) are chronic neurological diseases characterized by progressive neuronal loss and pathological protein deposition in specific brain regions. With the deepening of population aging, these diseases have become one of the most serious public health challenges. Due to the high heterogeneity of these disorders and the complex pathogenesis, it brings great challenges to clinical precision diagnosis and treatment. In this context, nuclear medicine molecular imaging technology represented by positron emission tomography (PET) and emerging radioactive ligand therapy (RLT) has achieved breakthrough development. This kind of technology can realize the visual detection of specific molecular pathological proteins ( β-amyloid (Aβ), Tau, α-synuclein) in vivo, and provide key information support for the accurate classification of pathological subtypes of NDs. This paper systematically reviews the research results of the whole process from the discovery of diagnostic biomarkers to the therapeutic intervention of nuclear medicine. At the same time, it discusses emerging frontiers, including AI‑assisted analysis and novel probe development. Despite substantial theoretical potential, these approaches face major translational barriers such as standardization and validation gaps. This review thus aims to provide an integrated perspective to facilitate ND translational breakthroughs.