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Rosalia C M Simmen Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA

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Dustin M Brown Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA

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Charles M Quick Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA

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Iad Alhallak Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA

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Tyler Rose Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA

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Shi J Liu Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA

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Angela S Kelley Department of Obstetrics and Gynecology, The University of Michigan Health System, Ann Arbor, Michigan, USA

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implicated in ENDO pathophysiology. Neutrophils, macrophages, and natural killer cells recruited to EC may promote ENDO in two ways. One mechanism for which the estrogen receptor-β (ESR2) signaling cascade has been implicated ( Han et al. 2015 ), results in

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-19-0248
Volume/Issue:
Volume 243: Issue 3
Free access
Samuel M Lee Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, USA

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Jose Muratalla Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, USA

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Marta Sierra-Cruz Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, USA

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Jose Cordoba-Chacon Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, USA

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-specific PPARγ-knockout mice lose both PPARγ isoforms. However, it should be known that aP2 is not only expressed in adipocytes but also in macrophages ( Furuhashi et al. 2008 ). The non-specificity of the aP2-Cre line, together with the high expression of

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-22-0155
Volume/Issue:
Volume 257: Issue 1
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Salla Nuutinen Research Center for Integrative Physiology and Pharmacology, and Turku Center for Disease Modeling, Institute of Biomedicine, University of Turku, Turku, Finland

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Liisa Ailanen Research Center for Integrative Physiology and Pharmacology, and Turku Center for Disease Modeling, Institute of Biomedicine, University of Turku, Turku, Finland

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Eriika Savontaus Research Center for Integrative Physiology and Pharmacology, and Turku Center for Disease Modeling, Institute of Biomedicine, University of Turku, Turku, Finland
Unit of Clinical Pharmacology, Turku University Hospital, Turku, Finland

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Petteri Rinne Research Center for Integrative Physiology and Pharmacology, and Turku Center for Disease Modeling, Institute of Biomedicine, University of Turku, Turku, Finland

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understanding, several factors, including hyperglycemia and hyperlipidemia, may cause endothelial dysfunction that is the initiating event of atherosclerosis. Endothelial dysfunction permits the infiltration of immune cells, mainly macrophages and T cells, and

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-17-0636
Volume/Issue:
Volume 236: Issue 3
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Morag J Young Baker Heart and Diabetes Institute, Prahran, Australia
Hudson Institute of Medical Research, Clayton, Australia

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Colin D Clyne Hudson Institute of Medical Research, Clayton, Australia

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Karen E Chapman The University/BHF Centre for Cardiovascular Science, The University of Edinburgh, The Queen’s Medical Research Institute, Edinburgh, UK

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, including lung, heart and vasculature, CNS, kidney and macrophages among others ( Azushima et al. 2020 ). Although this remains an active area of research, therapeutic regulation of local RAAS components has offered new options for cardiovascular and other

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-20-0260
Volume/Issue:
Volume 247: Issue 2
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Barbara J Clark Department of Biochemistry and Molecular Biology, and the Center for Genetics and Molecular Medicine, School of Medicine, University of Louisville, Louisville, Kentucky 40292, USA

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* † Cellular location Lipid binding Function/metabolic pathway STARD1/D3 STARD1 StAR Adrenal, ovary, testis, brain † Mitochondria ‡ ,a,b,c Cholesterol d,e Steroidogenesis 1 STARD3 MLN64 MENTAL-START Placenta, breast, macrophages * Transmembrane, late endosomes

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-11-0313
Volume/Issue:
Volume 212: Issue 3
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Brototi Roy Department of Zoology, University of Delhi, Delhi-110 007, India

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Rajeev Singh Department of Zoology, University of Delhi, Delhi-110 007, India

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Sunil Kumar Department of Zoology, University of Delhi, Delhi-110 007, India

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Umesh Rai Department of Zoology, University of Delhi, Delhi-110 007, India

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pronounced at the concentration present during night-time ( Terron et al . 2002 ). A similar effect on phagocytosis is seen in rat though the macrophages were isolated from testis ( Pawlak et al . 2005 ). As far as the direct evidence on the role of

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-08-0270
Volume/Issue:
Volume 199: Issue 3
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M Granado Departamento de Fisiología, Facultad de Medicina, Universidad Complutense, Madrid 28040, Spain

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A I Martín Departamento de Fisiología, Facultad de Medicina, Universidad Complutense, Madrid 28040, Spain

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T Priego Departamento de Fisiología, Facultad de Medicina, Universidad Complutense, Madrid 28040, Spain

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M A Villanúa Departamento de Fisiología, Facultad de Medicina, Universidad Complutense, Madrid 28040, Spain

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A López-Calderón Departamento de Fisiología, Facultad de Medicina, Universidad Complutense, Madrid 28040, Spain

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injury ( Hamada et al. 1999 ). For that reason, it has been postulated that Kupffer cells or hepatic macrophages mediate most of deleterious effect in liver injury. Gadolinium chloride is a Kupffer cell inhibitor. Use of gadolinium chloride is a

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.06585
Volume/Issue:
Volume 188: Issue 3
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Carsten T Herz Clinical Division of Endocrinology and Metabolism, Department of Medicine III, Medical University of Vienna, Vienna, Austria

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Florian W Kiefer Clinical Division of Endocrinology and Metabolism, Department of Medicine III, Medical University of Vienna, Vienna, Austria

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. Mechanistically, these effects were linked to lower expression of the key bacterial enzymes necessary for the lipid A biosynthesis, a critical lipopolysaccharide (LPS)-building component. Decreased LPS production was associated with anti-inflammatory M2 macrophage

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-18-0598
Volume/Issue:
Volume 241: Issue 3
Free access
Jiean Xu State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Qiuhua Yang State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Xiaoyu Zhang State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Zhiping Liu State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Yapeng Cao State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Lina Wang State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Yaqi Zhou State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Xianqiu Zeng State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Qian Ma State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Yiming Xu Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA
School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China

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Yong Wang Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA
College of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, China

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Lei Huang Department of Cardiovascular Surgery, Peking University Shenzhen Hospital, Shenzhen, China

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Zhen Han Department of Cardiovascular Surgery, Peking University Shenzhen Hospital, Shenzhen, China

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Tao Wang Department of Cardiovascular Surgery, Peking University Shenzhen Hospital, Shenzhen, China

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David Stepp Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Zsolt Bagi Department of Physiology, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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Chaodong Wu Department of Nutrition and Food Science, Texas A&M University, College Station, Texas, USA

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Mei Hong State Key Laboratory of Chemical Oncogenomics, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China

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Yuqing Huo Vascular Biology Center, Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, Georgia, USA

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the proinflammatory cytokines Tnfa and Ccl2 , and a marked increase in Mrc1 , a marker of M2 macrophages in the liver ( Fig. 4E and F ). Collectively, these results suggest that endothelial Adk deficiency attenuates HFD-induced hepatic

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-19-0126
Volume/Issue:
Volume 242: Issue 2
Free access
Xiaofeng Wang Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada T6G 2R3

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Catherine B Chan Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada T6G 2R3

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-cells in response to linoleic acid ( Salehi et al . 2005 ). In immune cells, GPR40 is only detected in monocytes ( Mancini & Poitout 2013 ). The macrophages are the main infiltrating inflammatory cells derived from monocytes in adipose tissue in obese and

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-14-0581
Volume/Issue:
Volume 224: Issue 3
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