AGING & DISEASE (A&D) 是一本同行评议的开放获取在线期刊，旨在发表关于衰老生物学、年龄相关疾病的病理生理学以及影响老年人疾病的创新疗法等核心问题的新颖且具有高影响力的研究结果人口。感兴趣的疾病包括（但不限于）中风、阿尔茨海默病、帕金森病、癫痫、痴呆、抑郁症、心血管疾病、癌症、关节炎、白内障、骨质疏松症、糖尿病和高血压。动物模型和人类研究欢迎组织或细胞。

Aging and Disease (A&D) is a peer-reviewed open-access online journal dedicated to publishing novel and impactful research findings on core issues related to aging biology, the pathophysiology of age-related diseases, and innovative therapies affecting diseases in older adults. The diseases of interest include, but are not limited to, stroke, Alzheimer's disease, Parkinson's disease, epilepsy, dementia, depression, cardiovascular diseases, cancer, arthritis, cataracts, osteoporosis, diabetes, and hypertension. We welcome submissions of both animal models and human studies.

《Aging and Disease》是一本经过同行评审的开放获取在线期刊，旨在发表关于衰老生物学、年龄相关疾病的病理生理学以及影响老年人疾病的创新疗法等核心问题的新颖且具有高影响力的研究成果。我们关注的疾病包括（但不限于）中风、阿尔茨海默病、帕金森病、癫痫、痴呆、抑郁症、心血管疾病、癌症、关节炎、白内障、骨质疏松症、糖尿病和高血压。我们欢迎动物模型和人类研究的投稿。

Aging and Disease

Ossification of the posterior longitudinal ligament (OPLL) is a multi-factorial disease involving an ectopic bone formation of spinal ligaments. It affects 0.8-3.0% aging Asian and 0.1-1.7% aging European Caucasian. The ossified ligament compresses nerve roots in the spinal cord and causes serious neurological problems such as myelopathy and radiculopathy. Research in understanding pathogenesis of OPLL over the past several decades have revealed many genetic and non-genetic factors contributing to the development and progress of OPLL. The characterizations of aberrant signaling of bone morphogenetic protein (BMP) and mitogen-activated protein kinases (MAPK), and the pathological phenotypes of OPLL-derived mesenchymal stem cells (MSCs) have provided new insights on the molecular mechanisms underlying OPLL. This paper reviews the recent progress in understanding the pathophysiology of OPLL and proposes future research directions on OPLL.

Liang Yan

Rui Gao

Yang Liu

Baorong He

Shemin Lv

Dingjun Hao

The Pathogenesis of Ossification of the Posterior Longitudinal Ligament

后纵韧带骨化的发病机制

Stroke is one of the most prevalent causes of death around the world. When a stroke occurs, many cellular signaling cascades and regulators are activated, which results in severe cellular dysfunction and debilitating long-term disability. One crucial regulator of cell fate and function is mammalian Forkhead box protein O1 (FoxO1). Many studies have found FoxO1 to be implicated in many cellular processes, including regulating gluconeogenesis and glycogenolysis. During a stroke, modifications of FoxO1 have been linked to a variety of functions, such as inducing cell death and inflammation, inhibiting oxidative injury, affecting the blood brain barrier (BBB), and regulating hepatic gluconeogenesis. For these functions of FoxO1, different measures and treatments were applied to FoxO1 after ischemia. However, the subtle mechanisms of post-transcriptional modification and the role of FoxO1 are still elusive and even contradictory in the development of stroke. The determination of these mechanisms will lead to further enlightenment for FoxO1 signal transduction and the identification of targeted drugs. The regulation and function of FoxO1 may provide an important way for the prevention and treatment of diseases. Overall, the functions of FoxO1 are multifactorial, and this paper will summarize all of the significant pathways in which FoxO1 plays an important role during stroke damage and recovery.

Sichao Guo

Ruchi Mangal

Chaitu Dandu

Xiaokun Geng

Yuchuan Ding

Role of Forkhead Box Protein O1 (FoxO1) in Stroke: A Literature Review

叉头框蛋白O1（FoxO1）在中风中的作用：文献综述

Patients with intracerebral hemorrhage (ICH) often suffer from heterogeneous long-term neurological deficits, such as cognitive decline. Our ability to measure secondary brain injury to predict the long-term outcomes of these patients is limited. We investigated whether the blood neurofilament light chain (NfL) can monitor brain injury and predict long-term outcomes in patients with ICH. We enrolled 300 patients with first-episode ICH within 24 h recruited in the Chinese Cerebral Hemorrhage Mechanisms and Intervention study cohort from January 2019 to June 2020. Patients were prospectively followed up for 12 months. Blood samples were collected from 153 healthy participants. Plasma NfL levels determined using a single-molecule array revealed a biphasic increase in plasma NfL in ICH patients compared to healthy controls, with the first peak at around 24 h and a second elevation from day 7 through day 14 post-ICH. Plasma NfL levels were positively correlated with hemorrhage volume, National Institute of Health Stroke Scale, and Glasgow Coma Scale scores of ICH patients. Higher NfL concentration within 72 h after ictus was independently associated with 6- and 12-month worsened functional outcomes (modified Rankin Scale ≥ 3) and higher all-cause mortality. Magnetic resonance imaging and cognitive function evaluation were available for 26 patients at 6 months post-ICH, and NfL levels measured 7 days post-ictus correlated with decreased white matter fiber integrity and poor cognitive function at 6 months after stroke. These findings suggest that blood NfL is a sensitive marker for monitoring axonal injury post-ICH and can predict long-term functional ability and survival.

Pei Zheng

Xuejiao Wang

Jingshan Chen

Xinli Wang

Samuel X Shi

Kaibin Shi

Plasma Neurofilament Light Chain Predicts Mortality and Long-Term Neurological Outcomes in Patients with Intracerebral Hemorrhage

血浆神经丝轻链预测脑出血患者的死亡率和长期神经功能结局

Hypoxia is an environmental stress at high altitude and underground conditions but it is also present in many chronic age-related diseases, where blood flow into tissues is impaired. The oxygen-sensing system stimulates gene expression protecting tissues against hypoxic insults. Hypoxia stabilizes the expression of hypoxia-inducible transcription factor-1α (HIF-1α), which controls the expression of hundreds of survival genes related to e.g. enhanced energy metabolism and autophagy. Moreover, many stress-related signaling mechanisms, such as oxidative stress and energy metabolic disturbances, as well as the signaling cascades via ceramide, mTOR, NF-κB, and TGF-β pathways, can also induce the expression of HIF-1α protein to facilitate cell survival in normoxia. Hypoxia is linked to prominent epigenetic changes in chromatin landscape. Screening studies have indicated that the stabilization of HIF-1α increases the expression of distinct histone lysine demethylases (KDM). HIF-1α stimulates the expression of KDM3A, KDM4B, KDM4C, and KDM6B, which enhance gene transcription by demethylating H3K9 and H3K27 sites (repressive epigenetic marks). In addition, HIF-1α induces the expression of KDM2B and KDM5B, which repress transcription by demethylating H3K4me2,3 sites (activating marks). Hypoxia-inducible KDMs support locally the gene transcription induced by HIF-1α, although they can also control genome-wide chromatin landscape, especially KDMs which demethylate H3K9 and H3K27 sites. These epigenetic marks have important role in the control of heterochromatin segments and 3D folding of chromosomes, as well as the genetic loci regulating cell type commitment, proliferation, and cellular senescence, e.g. the INK4 box. A chronic stimulation of HIF-1α can provoke tissue fibrosis and cellular senescence, which both are increasingly present with aging and age-related diseases. We will review the regulation of HIF-1α-dependent induction of KDMs and clarify their role in pathological processes emphasizing that long-term stress-related insults can impair the maintenance of chromatin landscape and provoke cellular senescence and tissue fibrosis associated with aging and age-related diseases.

Salminen Antero

Kaarniranta Kai

Kauppinen Anu

Aging and disease

Hypoxia-Inducible Histone Lysine Demethylases: Impact on the Aging Process and Age-Related Diseases

低氧诱导的组蛋白赖氨酸去甲基化酶：对衰老过程及年龄相关疾病的影响

Reactive astrocytes (RAs) produce chondroitin sulfate proteoglycans (CSPGs) in large quantities after spinal cord injury (SCI) and inhibit axon regeneration through the Rho-associated protein kinase (ROCK) pathway. However, the mechanism of producing CSPGs by RAs and their roles in other aspects are often overlooked. In recent years, novel generation mechanisms and functions of CSPGs have gradually emerged. Extracellular traps (ETs), a new recently discovered phenomenon in SCI, can promote secondary injury. ETs are released by neutrophils and microglia, which activate astrocytes to produce CSPGs after SCI. CSPGs inhibit axon regeneration and play an important role in regulating inflammation as well as cell migration and differentiation; some of these regulations are beneficial. The current review summarized the process of ET-activated RAs to generate CSPGs at the cellular signaling pathway level. Moreover, the roles of CSPGs in inhibiting axon regeneration, regulating inflammation, and regulating cell migration and differentiation were discussed. Finally, based on the above process, novel potential therapeutic targets were proposed to eliminate the adverse effects of CSPGs.

Rui Yang

Ying Zhang

Jianning Kang

Ce Zhang

Bin Ning

Chondroitin Sulfate Proteoglycans Revisited: Its Mechanism of Generation and Action for Spinal Cord Injury

硫酸软骨素蛋白聚糖再探讨：其生成机制与脊髓损伤作用

Runyu Liang

Qiang Tang

Jia Chen

Luwen Zhu

Epigenetic Clocks: Beyond Biological Age, Using the Past to Predict the Present and Future

表观遗传时钟：超越生物年龄，利用过去预测现在与未来

Haiyang Chen

Lijun Zhang

Meiyan Liu

Yanwei Li

Yunpeng Chi

Multi-Omics Research on Angina Pectoris: A Novel Perspective

心绞痛的多组学研究：一种新视角

Osteoarthritis (OA), a prevalent age-related disease, is increasingly recognized as a multifactorial condition. This comprehensive review provides a multifaceted perspective on the organ-joint crosstalk contributing to OA, transcending the traditional focus on local joint pathology. Based on current research, we discussed the brain-joint, gut-joint, muscle-joint interactions in the etiology and progression of OA. In brain-joint axis, the neuroendocrine regulation, circadian rhythms, and leptin signaling influence joint tissues. We also discussed the role of prostaglandin E2 in skeletal interoception and its potential as a therapeutic target. The gut-joint axis is underscored by the impact of gut microbiota dysbiosis on systemic inflammation and metabolic disorders, both of which are implicated in OA pathogenesis. Furthermore, age-related sarcopenia, characterized by muscle mass and strength loss, is identified as a significant risk factor. Sarcopenia may contribute to OA progression through compromised mechanical support, systemic inflammation, and muscle-derived myokines. Finally, we synthesize the evidence supporting the modulation of circadian rhythm, skeletal interoception, gut microbiome, and muscle mass as innovative strategies for OA management. The organ-joint crosstalk is integral to the complex pathogenesis of OA, highlighting the multifactorial nature of OA and the potential for targeted therapeutic interventions. By integrating these multidimensional perspectives, we aim to enhance our understanding of OA pathogenesis and explore potential pharmacological targets.

Dinglong Yang

Yujing Chen

Junfei Guo

Xin Xu

Mingyi Yang

Jiale Xie

Ke Xu

Peng Xu

The Organ-Joint Axes in Osteoarthritis: Significant Pathogenesis and Therapeutic Targets

骨关节炎中的器官-关节轴：重要的发病机制和治疗靶点

Cirrhosis incidence is significantly increased with age and frequently complicated with neurocognitive dysfunction. We have evaluated the contribution of aging to neuroinflammation in the liver-brain axis in advanced chronic liver disease. Young (6-week-old) and old (9-month-old) mice were included in a 12-week protocol of CCl

Sebastiań Martínez-López

María Salud García-Gutiérrez

Francisco Navarrete

Isabel Gómez-Hurtado

Pedro Zapater

Enrique Ańgel

Oriol Juanola

Juan L López-Cánovas

Paula Boix

Manel C Hadid

Amaya Puig-Kröger

Manuel D Gahete

Jorge Manzanares

Esther Caparrós

Rubén Francés

Aging Deteriorates Blood Brain Barrier Function and Polarizes Adaptive T Cell Expansion Contributing to Neurocognitive Damage in Experimental Cirrhosis

衰老损害血脑屏障功能并极化适应性T细胞扩增，从而导致实验性肝硬化中的神经认知损伤

With the progression of global aging, neurological diseases in elderly individuals have aroused widespread interest among researchers. Imbalances in the homeostasis of neuronal microenvironments, including neural progenitor cells and microglia, are the leading cause of worsening neurodegenerative diseases. The aging of various glial cells can further lead to abnormal functions in the central nervous system (CNS). Recent studies have shown that aging plays a vital role in a variety of degenerative diseases, including Huntington's disease (HD). In this manuscript, we describe the molecular mechanisms of aging, the cellular constitution of the neural microenvironment and the progression of aging in various neurodegenerative diseases, providing new targets and perspectives for the clinical treatment of various neurodegenerative diseases.

Dan Zhou

Yumeng Lin

Zhongyu Han

Zhuyun Zhang

Le Lin

Shichong Lin

Qianke Yang

The Impact of Aging on Neurological Diseases in the Elderly: Molecular Mechanisms and Therapeutic Perspectives

老龄化对老年人神经系统疾病的影响：分子机制与治疗展望

Abbreviation	Aging dis
Journal Impact	6.96
Quartiles(Global)	GERIATRICS & GERONTOLOGY(Q1)

ISSN	2152-5250
h-index	80

Publication Information	Publisher: International Society on Aging and Disease，Publishing cycle: ，Journal Type: journal，Open Access Journals: Yes
Basic data	Year of publication: 2010，Proportion of original research papers: 62.86%，Self Citation Rate:7.10%， Gold OA Rate: 89.82%
Journal Fees	$2000Details
Average review cycle	网友分享经验：10 Weeks

Aging and Disease

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