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Longitudinal assessment of peripheral organ metabolism and the gut microbiota in an APP/PS1 transgenic mouse model of Alzheimer’s disease

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Neural Regeneration Research 2025年第10期20卷 2982-2997页

作者： Hongli Li Jianhua Huang Di Zhao Lemei Zhu Zheyu Zhang Min Yi Weijun Peng department of Integrated Traditional Chinese&Western Medicine The Second Xiangya HospitalCentral South UniversityChangshaHunan ProvinceChina National Clinical Research Center for metabolic Diseases ChangshaHunan ProvinceChina Hunan Academy of Chinese Medicine ChangshaHunan ProvinceChina Academician Workstation Changsha Medical UniversityChangshaHunan ProvinceChina

Alzheimer’s disease not only affects the brain,but also induces metabolic dysfunction in peripheral organs and alters the gut *** aim of this study was to investigate systemic changes that occur in Alzheimer’s disease,in particular the association between changes in peripheral organ metabolism,changes in gut microbial composition,and Alzheimer’s disease *** do this,we analyzed peripheral organ metabolism and the gut microbiota in amyloid precursor protein-presenilin 1(APP/PS1)transgenic and control mice at 3,6,9,and 12 months of ***-month-old APP/PS1 mice exhibited cognitive impairment,Alzheimer’s disease-related brain changes,distinctive metabolic disturbances in peripheral organs and fecal samples(as detected by untargeted metabolomics sequencing),and substantial changes in gut microbial composition compared with younger APP/PS1 ***,a strong correlation emerged between the gut microbiota and kidney metabolism in APP/PS1 *** findings suggest that alterations in peripheral organ metabolism and the gut microbiota are closely related to Alzheimer’s disease development,indicating potential new directions for therapeutic strategies.

关键词： Alzheimer’s disease APP/PS1 mice brain-kidney axis gut microbiota heart-brain axis liver-brain axis lung-brain axis microbiota-gut-brain axis peripheral organ metabolism spleen-brain axis

Emerging evidence of the physiological role of hypoxia in mammary development and lactation

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Journal of Animal science and Biotechnology 2014年第3期5卷 262-272页

作者： Yong Shao Feng-Qi Zhao Laboratory of Lactation and metabolic Physiology Department of Animal ScienceUniversity of Vermont

Hypoxia is a physiological or pathological condition of a deficiency of oxygen supply in the body as a whole or within a tissue. During hypoxia, tissues undergo a series of physiological responses to defend themselves against a low oxygen supply, including increased angiogenesis, erythropoiesis, and glucose uptake. The effects of hypoxia are mainly mediated by hypoxia-inducible factor 1 （HIF-1）, which is a heterodimeric transcription factor consisting of o and 13 subunits. HIF-1β is constantly expressed, whereas HIF-1α is degraded under normal oxygen conditions. Hypoxia stabilizes HIF-1α and the HIF complex, and HIF then translocates into the nucleus to initiate the expression of target genes. Hypoxia has been extensively studied for its role in promoting tumor progression, and emerging evidence also indicates that hypoxia may play important roles in physiological processes, including mammary development and lactation. The mammary gland exhibits an increasing metabolic rate from pregnancy to lactation to support mammary growth, lactogenesis, and lactation. This process requires increasing amounts of oxygen consumption and results in localized chronic hypoxia as confirmed by the binding of the hypoxia marker pimonidazole HCI in mouse mammary gland. We hypothesized that this hypoxic condition promotes mammary development and lactation, a hypothesis that is supported by the following several lines of evidence： i） Mice with an HIF-1α deletion selective for the mammary gland have impaired mammary differentiation and lipid secretion, resulting in lactation failure and striking changes in milk compositions; ii） We recently observed that hypoxia significantly induces HIF-1α- dependent glucose uptake and GLUT1 expression in mammary epithelial cells, which may be responsible for the dramatic increases in glucose uptake and GLUT1 expression in the mammary gland during the transition period from late pregnancy to early lactation; and iii） Hypoxia and HIF-1α increase the phospho

关键词： Glucose transporter Hypoxia Hypoxia inducible factor Lactation Mammary development Metabolism

Timing of transplantation of autologous bone marrow derived mesenchymal stem cells for treating myocardial infarction

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science China(Life sciences) 2014年第2期57卷 195-200页

作者： CHEN YiHuan TENG XiaoMei CHEN WeiQian YANG JunJie YANG ZiYing YU YunSheng SHEN ZhenYa department of cardiovascular Surgery of the First Affiliated Hospital & Institute for cardiovascular science of Soochow University

It is still unclear whether the timing of intracoronary stem cell therapy affects the therapeutic response in patients with myocardial *** natural course of healing the infarction and the presence of putative homing signals within the damaged myocardium appear to favor cell engraftment during the transendothelial passage in the early days after ***,the adverse inflammatory environment,with its high oxidative stress,might be deleterious if cells are administered too early after *** we highlight several aspects of the timing of intracoronary stem cell *** results showed that transplantation of bone marrow mesenchymal stem cells at 2 4 weeks after myocardial infarction is more favorable for reduction of the scar area,inhibition of left ventricular remodeling,and recovery of heart *** injection of autologous bone marrow mesenchymal stem cells at 2 4 weeks after acute myocardial infarction is safe and does not increase the incidence of complications.

关键词： bone marrow mesenchymal stem cells(BMSCs) cell transplantation myocardial infarction

The mechanism and therapy of aortic aneurysms

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Signal Transduction and Targeted Therapy 2023年第3期8卷 963-982页

作者： Jianing Gao Huanhuan Cao Gaofei Hu Yufei Wu Yangkai Xu Hongtu Cui Hong S.Lu Lemin Zheng The Institute of cardiovascular sciences and Institute of Systems Biomedicine School of Basic Medical SciencesKey Laboratory of Molecular Cardiovascular Science of Ministry of EducationNHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory PeptidesBeijing Key Laboratory of Cardiovascular Receptors ResearchHealth Science CenterPeking University100191 BeijingChina department of Cardiology and Institute of Vascular Medicine Peking University Third HospitalNHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory PeptidesKey Laboratory of Molecular Cardiovascular ScienceMinistry of EducationBeijing Key Laboratory of Cardiovascular Receptors ResearchResearch Unit of Medical Science Research Management/Basic and Clinical Research of Metabolic Cardiovascular DiseasesChinese Academy of Medical Sciences100191 BeijingChina department of Physiology Saha Cardiovascular Research CenterUniversity of KentuckySouth LimestoneLexingtonKY 40536-0298USA

Aortic aneurysm is a chronic aortic disease affected by many *** it is generally asymptomatic,it poses a significant threat to human life due to a high risk of *** of its strong concealment,it is difficult to diagnose the disease in the early *** present,there are no effective drugs for the treatment of *** intervention and endovascular treatment are the only *** current studies have discovered that inflammatory responses as well as the production and activation of various proteases promote aortic aneurysm,the specific mechanisms remain *** are further exploring the pathogenesis of aneurysms to find new targets for diagnosis and *** better understand aortic aneurysm,this review elaborates on the discovery history of aortic aneurysm,main classification and clinical manifestations,related molecular mechanisms,clinical cohort studies and animal models,with the ultimate goal of providing insights into the treatment of this devastating *** underlying problem with aneurysm disease is weakening of the aortic wall,leading to progressive *** not treated in time,the aortic aneurysm eventually *** aortic aneurysm is a local enlargement of an artery caused by a weakening of the aortic *** disease is usually asymptomatic but leads to high mortality due to the risk of artery rupture.

关键词： aortic diagnosis drugs treatment

Precision cardiac targeting:empowering curcumin therapy through smart exosome-mediated drug delivery in myocardial infarction

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Regenerative Biomaterials 2024年第5期3卷 23-35页

作者： Ming Chen Shengnan Wang Yihuan Chen Han Shen Lei Chen Liang Ding Qingsong Tang Ziying Yang Weiqian Chen Zhenya Shen department of cardiovascular Surgery of the First Affiliated Hospital&Institute for cardiovascular science Suzhou Medical CollegeSoochow UniversitySuzhou 215006China

Nanoparticle-mediated drug delivery has emerged as a highly promising and effective therapeutic approach for addressing myocardial ***,clinical translation tends to be a failure due to low cardiac retention as well as liver and spleen entrapment in previous ***,we report a two-step exosome delivery system,which precludes internalization by the mononuclear phagocyte system before the delivery of therapeutic cardiac targeting exosomes(ExoCTP).Importantly,curcumin released by ExoCTP diminishes reactive oxygen species over-accumulation in ischemic myocardium,as well as serum levels of lactate dehydrogenase,malonyldialdehyde,superoxide dismutase and glutathione,indicating better antioxidant capacity than free ***,our strategy was proven to greatly potentiate the delivery and therapeutic efficacy of curcumin without systemic *** together,our smart exosome-mediated drug delivery strategy can serve either as therapeutics alone or in combination with other drugs for effective heart targeting and subsequent wound healing.

关键词： myocardial infarction exosome targeting mononuclear phagocyte system peptide

Exercise training attenuates angiotensinⅡ-induced cardiac fibrosis by reducing POU2F1 expression

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Journal of Sport and Health science 2023年第4期12卷 464-476页

作者： Na Feng Haiyi Yu Yueshen Wang Youyi Zhang Han Xiao Wei Gao department of Cardiology and Institute of Vascular Medicine Peking University Third HospitalNational Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory PeptidesKey Laboratory of Molecular Cardiovascular ScienceMinistry of EducationBeijing Key Laboratory of Cardiovascular Receptors ResearchBeijing 100191China Research Unit of Medical science Research Management/Basic and Clinical Research of metabolic cardiovascular Diseases Chinese Academy of Medical SciencesBeijing 100191China

Background:Exercise training protects against heart ***,the mechanism underlying the protective effect of exercise training on angiotensinⅡ(AngⅡ)-induced cardiac fibrosis remains ***:An exercise model involving C57BL/6N mice and 6 weeks of treadmill training was ***Ⅱ(1.44 mg/kg/day)was administered to induce cardiac *** sequencing and bioinformatic analysis were used to identify the key factors mediating the effects of exercise training on cardiac *** adult mouse cardiac fibroblasts(CFs)were used in ***-associated virus serotype 9 was used to overexpress POU domain,class 2,transcription factor 1(POU2F1)in ***:Exercise training attenuated AngⅡ-induced cardiac fibrosis and reversed 39 gene expression *** transcription factor regulating the largest number of these genes was *** to controls,POU2F1 was shown to be signififcantly upregulated by AngⅡ,which is itself reduced by exercise *** vivo,POU2F1 overexpression nullified the benefits of exercise training on cardiac *** CFs,POU2F1 promoted cardiac *** enhancer-binding proteinβ(C/EBPβ)was predicted to be the transcription factor of POU2F1and verified using a dual-luciferase reporter *** vivo,exercise training activated AMP-activated protein kinase(AMPK)and alleviated the increase in C/EBPβinduced by AngⅡ.In CFs,AMPK agonist inhibited the increase in C/EBPβand POU2F1 induced by Ang II,whereas AMPK inhibitor reversed this ***:Exercise training attenuates AngⅡ-induced cardiac fibrosis by reducing *** training inhibits POU2F1 by activating AMPK,which is followed by the downregulation of C/EBPβ,the transcription factor of POU2F1.

关键词： AMPK C/EBPβ Cardiac fibrosis Exercise POU2F1

Mitochondria as therapeutic targets for cancer stem cells

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World Journal of Stem Cells 2015年第2期7卷 418-427页

作者： In Sung Song Jeong Yu Jeong Seung Hun Jeong Hyoung Kyu Kim Kyung Soo Ko Byoung Doo Rhee Nari Kim Jin Han National Research Laboratory for Mitochondrial Signaling Department of PhysiologyCollege of MedicineCardiovascular and Metabolic Disease CenterInje University

Cancer stem cells(CSCs) are maintained by theirsomatic stem cells and are responsible for tumor initiation, chemoresistance, and metastasis. Evidence for the CSCs existence has been reported for a number of human cancers. The CSC mitochondria have been shown recently to be an important target for cancer treatment, but clinical significance of CSCs and their mitochondria properties remain unclear. Mitochondriatargeted agents are considerably more effective compared to other agents in triggering apoptosis of CSCs, as well as general cancer cells, via mitochondrial dysfunction. Mitochondrial metabolism is altered in cancer cells because of their reliance on glycolytic intermediates, which are normally destined for oxidative phosphorylation. Therefore, inhibiting cancer-specific modifications in mitochondrial metabolism, increasing reactive oxygen species production, or stimulating mitochondrial permeabilization transition could be promising new therapeutic strategies to activate cell death in CSCs as well, as in general cancer cells. This review analyzed mitochondrial function and its potential as a therapeutic target to induce cell death in CSCs. Furthermore, combined treatment with mitochondriatargeted drugs will be a promising strategy for the treatment of relapsed and refractory cancer.

关键词： Cancer stem cells Mitochondria Relapsedand refractory cancer Therapeutic target Mitochondrialenergy metabolism

Galectin-3-centered paracrine network mediates cardiac inflammation and fibrosis upon β-adrenergic insult

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science China(Life sciences) 2023年第5期66卷 1067-1078页

作者： Guomin Hu Jimin Wu Huijun Gu Xiangning Deng Wenli Xu Shan Feng Shuaixing Wang Yao Song Zhengda Pang Xiuling Deng Aleksandr E.Vendrov Nageswara R.Madamanchi Marschall S.Runge Xinyu Wang Youyi Zhang Han Xiao Erdan Dong department of Cardiology and Institute of Vascular Medicine Peking University Third HospitalNHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory PeptidesKey Laboratory of Molecular Cardiovascular ScienceMinistry of EducationBeijing Key Laboratory of Cardiovascular Receptors ResearchResearch Unit of Medical Science Research Management/Basic and Clinical Research of Metabolic Cardiovascular DiseasesChinese Academy of Medical SciencesBeijing 100191China department of Physiology and Pathophysiology Cardiovascular Research CenterSchool of Basic Medical SciencesXi’an Jiaotong University Health Science CenterXi’an 710061China department of Internal Medicine Frankel Cardiovascular CenterUniversity of MichiganAnn ArborMI48109USA Academy for Advanced Interdisciplinary Studies Peking UniversityBeijing 100087China

Rapid over-activation of β-adrenergic receptors (β-AR) following acute stress initiates cardiac inflammation and injury by activating interleukin-18 (IL-18),however,the process of inflammation cascades has not been fully *** present study aimed to determine the mechanisms of cardiac inflammatory amplification following acute sympathetic *** bioinformatics analysis,galectin-3 was identified as a potential key downstream effector of β-AR and IL-18 *** serum level of galectin-3 was positively correlated with norepinephrine or IL-18 in patients with chest *** the heart of mice treated with β-AR agonist isoproterenol (ISO,5 mg kg^(-1)),galectin-3 expression was upregulated markedly later than IL-18 activation,and Nlrp3^(-/-)and Il18^(-/-)mice did not show ISO-induced galectin-3 *** was further revealed that cardiomyocyte-derived IL-18 induced galectin-3 expression in macrophages following ISO ***,galectin-3deficiency suppressed ISO-induced cardiac inflammation and fibrosis without blocking ISO-induced IL-18 *** with a galectin-3 inhibitor,but not a β-blocker,one day after ISO treatment effectively attenuated cardiac inflammation and *** conclusion,galectin-3 is upregulated to exaggerate cardiac inflammation and injury following acute β-AR activation,a galectin-3 inhibitor effectively blocks cardiac injury one day after β-AR insult.

关键词： galectin-3 interleukin-18 β-adrenergic receptor macrophage inflammation fibrosis

Role of metabolic dysfunction and inflammation along the liver-brain axis in animal models with obesity-induced neurodegeneration

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Neural Regeneration Research 2025年第4期20卷 1069-1076页

作者： Evridiki Asimakidou Eka Norfaishanty Saipuljumri Chih Hung Lo Jialiu Zeng department of Clinical Neurosciences University of CambridgeCambridgeUK School of Applied science Republic PolytechnicSingaporeSingapore Lee Kong Chian School of Medicine Nanyang Technological UniversitySingaporeSingapore

The interaction between metabolic dysfunction and inflammation is central to the development of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s ***-related conditions like type 2 diabetes and non-alcoholic fatty liver disease exacerbate this *** lipid accumulation,particularly in the liver,initiates a cascade of inflammatory processes that extend to the brain,influencing critical metabolic regulatory *** and palmitate,key lipid components,along with lipid transporters lipocalin-2 and apolipoprotein E,contribute to neuroinflammation by disrupting blood–brain barrier integrity and promoting *** insulin resistance further exacerbates brain insulin resistance and *** interventions targeting peripheral lipid metabolism and insulin signaling pathways have shown promise in reducing neuroinflammation in animal ***,translating these findings to clinical practice requires further investigation into human *** conclusion,metabolic dysfunction,peripheral inflammation,and insulin resistance are integral to neuroinflammation and *** these complex mechanisms holds potential for identifying novel therapeutic targets and improving outcomes for neurodegenerative diseases.

关键词： Alzheimer’s disease inflammatory cytokines insulin resistance lipid