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Zheng Chen Department of Endocrinology and Metabolism, The Second Affiliated Hospital of Nanchang University, Nanchang, China

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Haixia Zeng Department of Endocrinology and Metabolism, The Second Affiliated Hospital of Nanchang University, Nanchang, China

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Qiulan Huang Department of Endocrinology and Metabolism, The Second Affiliated Hospital of Nanchang University, Nanchang, China

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Cuiping Lin Department of Endocrinology and Metabolism, The Second Affiliated Hospital of Nanchang University, Nanchang, China

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Xuan Li Department of Endocrinology and Metabolism, The Second Affiliated Hospital of Nanchang University, Nanchang, China

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Shaohua Sun Department of Endocrinology and Metabolism, The Second Affiliated Hospital of Nanchang University, Nanchang, China

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Jian-ping Liu Department of Endocrinology and Metabolism, The Second Affiliated Hospital of Nanchang University, Nanchang, China

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inflammation and lipid transport, inhibits complement proteins, and delays cell apoptosis ( 16 , 17 , 18 ). The downregulation of CLU expression leads to the increased expression of proinflammatory cytokines and ultimately leads to apoptosis ( 19 ). In a

Article Type:
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Reproduction
DOI:
https://doi.org/10.1530/EC-23-0428
Volume/Issue:
Volume 13: Issue 3
Open access
Enrique Pedernera Universidad Nacional Autónoma de México, Facultad de Medicina, Departamento de Embriología y Genética, Ciudad de México, México

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Flavia Morales-Vásquez Instituto Nacional de Cancerología, Ciudad de México, México

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María J Gómora Universidad Nacional Autónoma de México, Facultad de Medicina, Departamento de Embriología y Genética, Ciudad de México, México

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Miguel A Almaraz Universidad Nacional Autónoma de México, Facultad de Medicina, Departamento de Embriología y Genética, Ciudad de México, México

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Esteban Mena Universidad Nacional Autónoma de México, Facultad de Medicina, Secretaría General, Ciudad de México, México
Universidad La Salle, Posgrado de la Facultad de Ciencias Químicas, Ciudad de México, México

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Delia Pérez-Montiel Instituto Nacional de Cancerología, Ciudad de México, México

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Elizabeth Rendon Hospital Militar de Especialidades de la Mujer y Neonatología. Ciudad de México, México

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Horacio López-Basave Instituto Nacional de Cancerología, Ciudad de México, México

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Juan Maldonado-Cubas Universidad La Salle, Posgrado de la Facultad de Ciencias Químicas, Ciudad de México, México

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Carmen Méndez Universidad Nacional Autónoma de México, Facultad de Medicina, Departamento de Embriología y Genética, Ciudad de México, México

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considered; the receptor is regulated by E2, and clinical studies have shown it to be a protective factor ( 34 ). In addition, progesterone in vitro reduces cell number and increases apoptosis in ovarian cancer cells ( 35 , 36 ). There is also a need to

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Hormones and Cancer
DOI:
https://doi.org/10.1530/EC-23-0315
Volume/Issue:
Volume 12: Issue 12
Open access
Jiaxin Zhang Department of Traditional Chinese Medicine (TCM) Orthopedics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Jinlan Jiang Wenzhou Institute, University of Chinese Academy of Sciences, Wenzhou, Zhejiang, China

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Yao Qin School of Public Health, Hangzhou Medical College, Hangzhou, Zhejiang, China

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Yihui Zhang Department of Traditional Chinese Medicine (TCM) Orthopedics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Yungang Wu Department of Traditional Chinese Medicine (TCM) Orthopedics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Huadong Xu School of Public Health, Hangzhou Medical College, Hangzhou, Zhejiang, China

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apoptosis of bone mesenchymal stem cells and osteoblasts through oxidative stress, which is related to the pathogenesis of osteoporosis ( 8 , 9 ). The systemic immune-inflammation index (SII) is a new inflammatory index based on peripheral blood neutrophils

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Bone and Mineral Metabolism
DOI:
https://doi.org/10.1530/EC-22-0461
Volume/Issue:
Volume 12: Issue 2
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Fernando Aprile-Garcia Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina
Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina

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María Antunica-Noguerol Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina
Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina

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Maia Ludmila Budziñski Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina

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Ana C Liberman Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina

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Eduardo Arzt Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina
Instituto de Investigación en Biomedicina de Buenos Aires – CONICET, Departamento de Fisiología, Partner Institute of the Max Planck Society, Buenos Aires, Argentina

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receiving considerable attention. PARP1 has been shown to be involved in different injury mechanisms affecting neurons. As previously described for GC-mediated apoptosis (30) , it is already recognized that PARP1-mediated cell death is one of the dominant

Article Type:
Review Article
DOI:
https://doi.org/10.1530/EC-13-0079
Volume/Issue:
Volume 3: Issue 1
Open access
Kate E Lines Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Mahsa Javid Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Anita A C Reed Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Gerard V Walls Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Mark Stevenson Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Michelle Simon MRC Harwell Institute, Mammalian Genetics Unit, Harwell Campus, Oxfordshire, UK

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Kreepa G Kooblall Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Sian E Piret Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Paul T Christie Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Paul J Newey Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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Ann-Marie Mallon MRC Harwell Institute, Mammalian Genetics Unit, Harwell Campus, Oxfordshire, UK

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Rajesh V Thakker Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), Churchill Hospital, Headington, Oxford, UK

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oncogene homologue ( Kras )); wnt signalling (wingless-type MMTV integration site family member 2B ( Wnt2b )); interleukin signalling (Interleukin-3 receptor subunit alpha ( Il3ra )) and apoptosis signalling (TNF receptor superfamily member 10a ( Tnfrsf10a

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-20-0103
Volume/Issue:
Volume 9: Issue 5
Open access
Sylvia Thiele Department of Medicine III, Technische Universität Dresden, Dresden, Germany
Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany

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Anke Hannemann Institute of Clinical Chemistry and Laboratory Medicine, University Medicine Greifswald, Greifswald, Germany

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Maria Winzer Department of Medicine III, Technische Universität Dresden, Dresden, Germany
Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany

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Ulrike Baschant Department of Medicine III, Technische Universität Dresden, Dresden, Germany
Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany

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Heike Weidner Department of Medicine III, Technische Universität Dresden, Dresden, Germany
Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany

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Matthias Nauck Institute of Clinical Chemistry and Laboratory Medicine, University Medicine Greifswald, Greifswald, Germany

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Rajesh V Thakker Academic Endocrine Unit, Radcliffe Department of Medicine University of Oxford, Oxford Centre for Diabetes, Endocrinology, and Metabolism, Churchill Hospital, Oxford, UK

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Martin Bornhäuser Department of Medicine I, Technische Universität Dresden, Dresden, Germany
DFG Research Center and Cluster of Excellence for Regenerative Therapies, Technical University, Dresden, Germany

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Lorenz C Hofbauer Department of Medicine III, Technische Universität Dresden, Dresden, Germany
Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany
DFG Research Center and Cluster of Excellence for Regenerative Therapies, Technical University, Dresden, Germany

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Martina Rauner Department of Medicine III, Technische Universität Dresden, Dresden, Germany
Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany

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) ratio in osteoblastic cells promotes osteoclastogenesis, inhibition of osteoblast differentiation, reduced matrix production, increased osteoblast and osteocyte apoptosis and increased autophagy further seem to contribute to GIO ( 5 , 6 , 7 , 8

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DOI:
https://doi.org/10.1530/EC-19-0104
Volume/Issue:
Volume 8: Issue 7
Open access
E T Aristizabal Prada Department of Internal Medicine IV, Campus Grosshadern, University-Hospital, Ludwig-Maximilians-University of Munich, Munich, Germany

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C J Auernhammer Department of Internal Medicine IV, Campus Grosshadern, University-Hospital, Ludwig-Maximilians-University of Munich, Munich, Germany

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MK-2206 in NET cell lines demonstrated a decrease in pAKT expression, inhibition of proliferation and induction of apoptosis mechanisms and a decreased expression of the NET tumour markers CgA and NSE ( 79 ). In a clinical phase 1 study with MK-2206

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DOI:
https://doi.org/10.1530/EC-17-0286
Volume/Issue:
Volume 7: Issue 1
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Legh Wilkinson Department of Biochemistry, Stellenbosch University, Stellenbosch, South Africa

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Nicolette J D Verhoog Department of Biochemistry, Stellenbosch University, Stellenbosch, South Africa

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Ann Louw Department of Biochemistry, Stellenbosch University, Stellenbosch, South Africa

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, 73 , 74 ) Rodents Experimental encephalomyelitis (EAE) T cells Reduced Reduced GC-resistant apoptosis ( 77 ) Cancer Human Acute lymphoblastic leukaemia (ALL)Multiple myeloma (MM)Small-cell lung cancer (SCLC), non

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https://doi.org/10.1530/EC-18-0421
Volume/Issue:
Volume 7: Issue 12
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Simonetta Piana Pathology Unit, Azienda USL – IRCCS Reggio Emilia, Reggio Emilia, Italy

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Eleonora Zanetti Pathology Unit, Azienda USL – IRCCS Reggio Emilia, Reggio Emilia, Italy

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Alessandra Bisagni Pathology Unit, Azienda USL – IRCCS Reggio Emilia, Reggio Emilia, Italy

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Alessia Ciarrocchi Laboratory of Translational Research, Azienda USL – IRCCS Reggio Emilia, Reggio Emilia, Italy

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Davide Giordano Otolaryngology Unit, Azienda USL – IRCCS Reggio Emilia, Reggio Emilia, Italy

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Federica Torricelli Laboratory of Translational Research, Azienda USL – IRCCS Reggio Emilia, Reggio Emilia, Italy

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Teresa Rossi Laboratory of Translational Research, Azienda USL – IRCCS Reggio Emilia, Reggio Emilia, Italy

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Moira Ragazzi Pathology Unit, Azienda USL – IRCCS Reggio Emilia, Reggio Emilia, Italy

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T Cao XT . NOTCH1 signaling inhibits growth of human hepatocellular carcinoma through induction of cell cycle arrest and apoptosis . Cancer Research 2003 63 . 10 Wang Z Da Silva TG Jin K Han X Ranganathan P Zhu X Sanchez

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https://doi.org/10.1530/EC-19-0303
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Volume 8: Issue 8
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Pamela Stratton Office of the Clinical Director, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA

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Neelam Giri Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA

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Sonia Bhala Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA

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Martha M Sklavos Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, Maryland, USA

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Blanche P Alter Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA

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Sharon A Savage Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA

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Ligia A Pinto Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, Maryland, USA

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, cell cycle, cell differentiation, and apoptosis, as well as the apoptotic regression of Müllerian ducts (fallopian tubes, uterus, cervix, and upper 1/3 of the vagina) in male fetuses. The normal male reproductive tract develops in utero in response to

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Reproduction
DOI:
https://doi.org/10.1530/EC-23-0510
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Volume 13: Issue 9
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