James Chapman

ORCID: 0000-0002-2841-282X
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About
Contact & Profiles
Research Areas
  • Telomeres, Telomerase, and Senescence
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Cancer therapeutics and mechanisms
  • Mitochondrial Function and Pathology
  • Genetics, Aging, and Longevity in Model Organisms
  • Cardiac Fibrosis and Remodeling
  • interferon and immune responses
  • Advanced NMR Techniques and Applications
  • ATP Synthase and ATPases Research
  • Ubiquitin and proteasome pathways
  • CRISPR and Genetic Engineering
  • Cardiac Ischemia and Reperfusion
  • Calpain Protease Function and Regulation
  • Cardiovascular Function and Risk Factors
  • Myasthenia Gravis and Thymoma
  • Metabolism and Genetic Disorders
  • Adipokines, Inflammation, and Metabolic Diseases
  • Cutaneous lymphoproliferative disorders research
  • Retinal Development and Disorders
  • Circadian rhythm and melatonin
  • Adipose Tissue and Metabolism
  • Autoimmune and Inflammatory Disorders
  • RNA regulation and disease
  • Emergency and Acute Care Studies
  • Cytomegalovirus and herpesvirus research

Newcastle University
2018-2024

Newcastle Hospitals - Campus for Ageing and Vitality
2018-2024

Wellcome Centre for Mitochondrial Research
2020-2022

Ochsner Medical Center
2005

Imperial College London
1999

Augusta University
1988

Oak Ridge National Laboratory
1985

George Washington University
1954

Abstract Senescent cells drive age-related tissue dysfunction partially through the induction of a chronic senescence-associated secretory phenotype (SASP) 1 . Mitochondria are major regulators SASP; however, underlying mechanisms have not been elucidated 2 often essential for apoptosis, cell fate distinct from cellular senescence. During widespread mitochondrial outer membrane permeabilization (MOMP) commits to die 3 Here we find that MOMP occurring in subset mitochondria is feature This...

10.1038/s41586-023-06621-4 article EN cc-by Nature 2023-10-11

Article25 March 2021Open Access Source DataTransparent process Neutrophils induce paracrine telomere dysfunction and senescence in ROS-dependent manner Anthony Lagnado Department of Physiology Biomedical Engineering, Mayo Clinic, Rochester, MN, USA Robert Arlene Kogod Center on Aging, Search for more papers by this author Jack Leslie Newcastle Fibrosis Research Group, Biosciences Institute, University, upon Tyne, UK Marie-Helene Ruchaud-Sparagano Translational Stella Victorelli Petra Hirsova...

10.15252/embj.2020106048 article EN cc-by The EMBO Journal 2021-03-25

Abstract A key component of cardiac ischemia–reperfusion injury (IRI) is the increased generation reactive oxygen species, leading to enhanced inflammation and tissue dysfunction in patients following intervention for myocardial infarction. In this study, we hypothesized that oxidative stress, due ischemia–reperfusion, induces senescence which contributes pathophysiology IRI. We demonstrate IRI cellular both cardiomyocytes interstitial cell populations treatment with senolytic drug...

10.1111/acel.13249 article EN cc-by Aging Cell 2020-09-29

Increased activation of the major pro-inflammatory NF-κB pathway leads to numerous age-related diseases, including chronic liver disease (CLD). Rapamycin, an inhibitor mTOR, extends lifespan and healthspan, potentially via suppression inflammaging, a process which is partially dependent on signalling. However, it unknown if rapamycin has beneficial effects in context compromised signalling, such as that occurs several diseases. In this study, we investigated whether could ameliorate...

10.1111/acel.12882 article EN cc-by Aging Cell 2018-11-23

Left ventricular hypertrophy (LVH) is more prevalent in black than white hypertensives, but this difference greater when identified by electrocardiography (ECG) echocardiography. We evaluated the proposal that current ECG criteria for LVH are less specific, and therefore, useful, blacks whites. In a retrospective cross-sectional study, 408 subjects (271 white, 137 black) referred to hypertension clinic assessment of underwent measurement blood pressure, voltages (Sokolow-Lyon Cornell...

10.1016/s0895-7061(99)00027-8 article EN American Journal of Hypertension 1999-05-01

Abstract Genetic processes require the activity of multiple topoisomerases, essential enzymes that remove topological tension and intermolecular linkages in DNA. We have investigated subcellular localisation six human topoisomerases with a view to understanding maintenance mitochondrial Our results indicate mitochondria contain two TOP1MT TOP3A. Using molecular, genomic biochemical methods we find both proteins contribute mtDNA replication, addition decatenation role TOP3A, is stimulated by...

10.1093/nar/gkac857 article EN cc-by Nucleic Acids Research 2022-09-26

Abstract Ageing is the biggest risk factor for cardiovascular health and associated with increased incidence of disease. Cellular senescence, a process driven in part by telomere shortening, has been implicated age-related tissue dysfunction. Here, we address question how senescence induced rarely dividing/post-mitotic cardiomyocytes investigate if clearance senescent cells attenuates age related cardiac During ageing, human murine acquire senescent-like phenotype characterised persistent...

10.1101/394809 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2018-08-17

Our website uses cookies to enhance your experience. By continuing use our site, or clicking "Continue," you are agreeing Cookie Policy | Continue JAMA Dermatology HomeNew OnlineCurrent IssueFor Authors Podcast Publications Network Open Cardiology Health Forum Internal Medicine Neurology Oncology Ophthalmology Otolaryngology–Head & Neck Surgery Pediatrics Psychiatry Archives of (1919-1959) JN Learning / CMESubscribeJobsInstitutions LibrariansReprints Permissions Terms Use Privacy...

10.1001/archderm.140.3.353-c article EN Archives of Dermatology 2004-03-01

Abstract Senescent cells drive age-related tissue dysfunction partially via the induction of a chronic senescence-associated secretory phenotype (SASP). Mitochondria are major regulators SASP; however, underlying mechanisms have not been elucidated. also control apoptosis, cell fate generally perceived as distinct from cellular senescence, which is apoptosis resistant. Here, we show that mitochondrial outer membrane permeability (MOMP) occurring in small subset mitochondria feature...

10.21203/rs.3.rs-1247316/v1 preprint EN cc-by Research Square (Research Square) 2022-03-10

Abstract A key component of cardiac ischemia-reperfusion injury (IRI) is the increased generation reactive oxygen species, leading to enhanced inflammation and tissue dysfunction in patients following intervention for myocardial infarction. In this study we hypothesized that oxidative stress, due ischemia-reperfusion, induces senescence which contributes pathophysiology IRI. We demonstrate IRI cellular both cardiomyocytes interstitial cell populations treatment with senolytic drug navitoclax...

10.1101/2020.04.28.065789 preprint EN cc-by bioRxiv (Cold Spring Harbor Laboratory) 2020-04-28

The sudden onset of symptomatic hemorrhoid disease in a 43 year old man heralded infrarenal aortic thrombosis after minor fall. He developed classic Leriche Syndrome and required thrombectomy aorto-bifemoral grafting. unusual presentation is explained by the collateral circulation arteriograms demonstrating this point are presented. It was felt that pres ence pre-existing sub-occlusive iliac predisposed patient to successful outcome followed surgical treatment.

10.1177/153857448501900308 article EN Vascular Surgery 1985-05-01
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