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  1. Article ; Online: What is hidden behind a pulmonary hypertensive, fibrotic and inflammatory phenotype?

    Adnot, Serge / Lipskaia, Larissa / Bischof, Oliver

    The European respiratory journal

    2022  Volume 60, Issue 4

    MeSH term(s) Animals ; Mice ; Pulmonary Fibrosis ; Pyridones ; Phenotype ; Scleroderma, Systemic
    Chemical Substances pirfenidone (D7NLD2JX7U) ; Pyridones
    Language English
    Publishing date 2022-10-20
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/13993003.01301-2022
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  2. Article: Sénescence cellulaire et physiopathologie des maladies respiratoires chroniques : rôle dans la bronchopneumopathie chronique obstructive.

    Adnot, Serge

    Bulletin de l'Academie nationale de medecine

    2014  Volume 198, Issue 4-5, Page(s) 659–671

    Abstract: Knowledge of the biology of cellular senescence has improved markedly in recent years, helping us to understand the aging process. It is now clear that cellular senescence is involved in the pathogenesis of many age-related diseases, including ... ...

    Title translation Cell senescence and pathophysiology of chronic lung diseases: role in chronic obstructive pulmonary disease.
    Abstract Knowledge of the biology of cellular senescence has improved markedly in recent years, helping us to understand the aging process. It is now clear that cellular senescence is involved in the pathogenesis of many age-related diseases, including respiratory diseases such as chronic obstructive pulmonary disease (COPD). COPD occupies a special place among chronic respiratory diseases because of its frequency and socio-economic impact. The high morbidity and mortality associated with COPD are related to multiple systemic manifestations independent of the severity of airway obstruction. COPD, although most often due to smoking, is also an aging-related respiratory disease. According to a newly developed concept, lung-cell senescence could play a key role in the pathophysiology of COPD, including remodeling of blood vessels and lung parenchyma, as well as the characteristic inflammatory process. Systemic manifestations of COPD, including cardiovascular disease, weight loss, bone demineralization and muscle dysfunction, may reflect a general process of premature aging secondary to the pulmonary changes.
    MeSH term(s) Aging/pathology ; Alveolar Epithelial Cells/pathology ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/physiopathology ; Cellular Microenvironment ; Cellular Senescence ; Comorbidity ; Cytokines/physiology ; Emphysema/complications ; Emphysema/physiopathology ; Genetic Predisposition to Disease ; Humans ; Hypertension, Pulmonary/physiopathology ; Inflammation ; Intercellular Signaling Peptides and Proteins/physiology ; Lung/pathology ; Models, Biological ; Muscular Diseases/epidemiology ; Muscular Diseases/physiopathology ; Peptide Hydrolases/physiology ; Pulmonary Disease, Chronic Obstructive/epidemiology ; Pulmonary Disease, Chronic Obstructive/etiology ; Pulmonary Disease, Chronic Obstructive/pathology ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Telomere Shortening
    Chemical Substances Cytokines ; Intercellular Signaling Peptides and Proteins ; Peptide Hydrolases (EC 3.4.-)
    Language French
    Publishing date 2014-04
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 213227-8
    ISSN 0001-4079
    ISSN 0001-4079
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: mTOR: A Key to Both Pulmonary Vessel Remodeling and Right Ventricular Function in Pulmonary Arterial Hypertension?

    Houssaini, Amal / Adnot, Serge

    American journal of respiratory cell and molecular biology

    2017  Volume 57, Issue 5, Page(s) 509–511

    Language English
    Publishing date 2017-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2017-0245ED
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The STATus of STAT3 in Lung Cell Senescence?

    Adnot, Serge / Lipskaia, Larissa / Bernard, David

    American journal of respiratory cell and molecular biology

    2019  Volume 61, Issue 1, Page(s) 5–6

    MeSH term(s) Cellular Senescence ; Fibroblasts/drug effects ; Oxidants ; STAT3 Transcription Factor
    Chemical Substances Oxidants ; STAT3 Transcription Factor
    Language English
    Publishing date 2019-02-26
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2019-0013ED
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  5. Article ; Online: PAI-1: A New Target for Controlling Lung-Cell Senescence and Fibrosis?

    Adnot, Serge / Breau, Marielle / Houssaini, Amal

    American journal of respiratory cell and molecular biology

    2019  Volume 62, Issue 3, Page(s) 271–272

    MeSH term(s) Cellular Senescence ; Fibrosis ; Humans ; Macrophages, Alveolar ; Plasminogen Activator Inhibitor 1 ; Transforming Growth Factor beta1
    Chemical Substances Plasminogen Activator Inhibitor 1 ; Transforming Growth Factor beta1
    Language English
    Publishing date 2019-10-17
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2019-0341ED
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Le traitement antioxydant protège contre l’emphysème mais favorise la survenue et la progression du cancer du poumon.

    Breau, Marielle / Bernard, David / Mechta-Grigoriou, Fatima / Adnot, Serge

    Medecine sciences : M/S

    2020  Volume 36, Issue 3, Page(s) 200–203

    Title translation Antioxidant treatment promotes lung cancer while protecting against lung emphysema.
    MeSH term(s) Acetylcysteine/adverse effects ; Acetylcysteine/therapeutic use ; Animals ; Antioxidants/adverse effects ; Antioxidants/therapeutic use ; Cell Transformation, Neoplastic/chemically induced ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/pathology ; Cellular Senescence/drug effects ; Cellular Senescence/genetics ; Cytoprotection/drug effects ; Cytoprotection/genetics ; Humans ; Lung/cytology ; Lung/drug effects ; Lung/metabolism ; Lung Neoplasms/chemically induced ; Lung Neoplasms/genetics ; Mice ; Mice, Knockout ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Proto-Oncogene Proteins c-jun/genetics ; Proto-Oncogene Proteins c-jun/physiology ; Pulmonary Emphysema/prevention & control
    Chemical Substances Antioxidants ; JunD protein, human ; Proto-Oncogene Proteins c-jun ; junD protein, mouse ; Acetylcysteine (WYQ7N0BPYC)
    Language French
    Publishing date 2020-03-31
    Publishing country France
    Document type News
    ZDB-ID 632733-3
    ISSN 1958-5381 ; 0767-0974
    ISSN (online) 1958-5381
    ISSN 0767-0974
    DOI 10.1051/medsci/2020030
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    Zs.B 2872: Show issues Location:
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  7. Article ; Online: Telomere shortening during human septic shock: influence of sepsis mediators, role in organ failures, and septic myocardial dysfunction.

    Razazi, Keyvan / Marcos, Elisabeth / Hüe, Sophie / Boyer, Laurent / Adnot, Serge / Mekontso Dessap, Armand

    Critical care (London, England)

    2021  Volume 25, Issue 1, Page(s) 401

    MeSH term(s) Cardiomyopathies ; Humans ; Multiple Organ Failure ; Sepsis ; Shock, Septic/genetics ; Shock, Septic/physiopathology ; Telomere Shortening
    Language English
    Publishing date 2021-11-18
    Publishing country England
    Document type Journal Article
    ZDB-ID 2041406-7
    ISSN 1466-609X ; 1364-8535
    ISSN (online) 1466-609X
    ISSN 1364-8535
    DOI 10.1186/s13054-021-03818-9
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    Zs.A 5517: Show issues Location:
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  8. Article ; Online: Anthracycline cardiotoxicity: looking for new therapeutic approaches targeting cell senescence?

    Abid, Shariq / Lipskaia, Larissa / Adnot, Serge

    Cardiovascular research

    2018  Volume 114, Issue 10, Page(s) 1304–1305

    MeSH term(s) Animals ; Anthracyclines ; Antibiotics, Antineoplastic ; Cellular Senescence ; Doxorubicin ; Mice ; Resveratrol
    Chemical Substances Anthracyclines ; Antibiotics, Antineoplastic ; Doxorubicin (80168379AG) ; Resveratrol (Q369O8926L)
    Language English
    Publishing date 2018-05-01
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvy108
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    Zs.A 565: Show issues Location:
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  9. Article: Lessons learned from cancer may help in the treatment of pulmonary hypertension.

    Adnot, Serge

    The Journal of clinical investigation

    2005  Volume 115, Issue 6, Page(s) 1461–1463

    Abstract: Hyperplasia of pulmonary artery SMCs (PASMCs) is a pathological hallmark of pulmonary arterial hypertension (PAH). In this issue of the JCI, McMurtry et al. report that adenovirus-mediated overexpression of survivin--a multipotent inhibitor of apoptosis-- ...

    Abstract Hyperplasia of pulmonary artery SMCs (PASMCs) is a pathological hallmark of pulmonary arterial hypertension (PAH). In this issue of the JCI, McMurtry et al. report that adenovirus-mediated overexpression of survivin--a multipotent inhibitor of apoptosis--induces PAH in rats, whereas inhalation of an adenovirus vector encoding a mutant survivin gene with dominant-negative properties reverses established monocrotaline-induced PAH. These findings raise important issues regarding the role of survivin in the pathogenesis of PAH, its value as a prognostic indicator, and its use as a target for new therapeutic strategies.
    MeSH term(s) Animals ; Apoptosis/genetics ; Genes, Dominant ; Genetic Therapy/methods ; Hypertension, Pulmonary/chemically induced ; Hypertension, Pulmonary/genetics ; Hypertension, Pulmonary/therapy ; Inhibitor of Apoptosis Proteins ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Mutation ; Neoplasm Proteins ; Neoplasms/genetics ; Neoplasms/metabolism ; Pulmonary Artery/metabolism ; Rats
    Chemical Substances BIRC5 protein, human ; Inhibitor of Apoptosis Proteins ; Microtubule-Associated Proteins ; Neoplasm Proteins
    Language English
    Publishing date 2005-06
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI25399
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Combined effects of smoking and HIV infection on the occurrence of aging-related manifestations.

    Boyer, Laurent / Zebachi, Sonia / Gallien, Sébastien / Margarit, Laurent / Ribeiro Baptista, Bruno / Lopez-Zaragoza, José-Luis / D'Humières, Thomas / Zerah, Françoise / Hue, Sophie / Derumeaux, Geneviève / Adnot, Serge / Audureau, Etienne / Lelièvre, Jean-Daniel

    Scientific reports

    2023  Volume 13, Issue 1, Page(s) 21745

    Abstract: Both HIV-1 infection and smoking may contribute to the development of ageing-related manifestations affecting the prognosis of people living with HIV, but it is unclear whether HIV and smoking exert their effects independently or interact by potentiating ...

    Abstract Both HIV-1 infection and smoking may contribute to the development of ageing-related manifestations affecting the prognosis of people living with HIV, but it is unclear whether HIV and smoking exert their effects independently or interact by potentiating each other. We conducted a cross-sectional study in 192 people living with HIV aged- and gender-matched with 192 HIV-uninfected controls, assessing the relative effect of HIV-1/smoking status on lung function (FEV1), bone mineral density (BMD), appendicular skeletal muscle mass index (ASMI), aortic pulse-wave velocity (PWV), insulin resistance (HOMA-IR) and renal function. In both unadjusted and adjusted analyses, FEV1, BMD and ASMI significantly differed according to smoking/HIV status, with the worst parameters found in HIV-1 infected patients currently smoking, and BMD and ASMI decreased to a lesser extent in HIV-1 infected patients formerly smoking (> 10 pack-years). Values in people living with HIV with < 10 pack-years exposure were of similar magnitude to those from controls. Regarding PWV, HOMA-R and eGFR, no significant differences were found, with the exception of eGFR values which were globally lower in HIV-1 infected patients. In conclusion HIV infection and smoking acted synergistically and were associated with a wasting phenotype combining muscle mass and bone mineral reduction.Clinical Trial Registration (registrar, website, and registration number), where applicable: CPP 10-023, 09-027, 10-034.
    MeSH term(s) Humans ; Aged ; HIV Infections/complications ; HIV Infections/epidemiology ; Smoking/adverse effects ; Cross-Sectional Studies ; Aging ; Tobacco Smoking ; HIV Seropositivity/complications ; Bone Density
    Language English
    Publishing date 2023-12-08
    Publishing country England
    Document type Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-023-39861-5
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