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Dr Jason Johnson

Dr Jason Johnson

Dr Jason Johnson
MSc, PhD

Reader of Cardiovascular Pathology

Area of research

Pathology of cardiovascular diseases including atherosclerosis, aortic aneurysms, restenosis, and adverse post-myocardial infarction remodelling

Office Room 85
Level 7,
Bristol Royal Infirmary, Upper Maudlin Street BS2 8HW
(See a map)

+44 (0) 117 34 23583

Summary

Dr Jason Johnson is a British Heart Foundation Senior Research Fellow and leads the Laboratory of Cardiovascular Pathology at the University of Bristol.

He has a long-standing interest in the pathophysiology of numerous cardiovascular pathologies including atherosclerosis, aortic aneurysms, and restenosis. His studies include a marriage of basic science and translational cardiovascular research with the goal of facilitating the development and deployment of novel therapies to combat the aforementioned cardiovascular diseases, alongside the identification of potential biomarkers of disease progression.

Since gaining his PhD in 2005, Dr Johnson’s research has underpinned the dogma that not all matrix metalloproteinases (MMPs) play detrimental roles in atherosclerotic plaque progression. Moreover, he has aided the identification of a macrophage phenotype (under the control of GM-CSF) which is characterised by high MMP-12 and MMP-14 protein expression alongside low TIMP-3 levels. Further work has also identified a novel node of microRNA regulation within GM-CSF macrophages, highlighting several potential new therapeutic avenues, including miR-181b inhibition and the selective inhibition of MMP-12. Collectively, these studies have made a major contribution to understanding the role of matrix metalloproteinases and macrophage heterogeneity in atherosclerotic plaque progression. Supporting studies in human aneurysm samples and pertinent pre-clinical in vivo models has reaffirmed the notion that the proteolytic profile of macrophage subsets predicts aneurysm development and progression. These findings are now being tested in a novel ex vivo human model of aneurysm that will hopefully supplant the requirement for animal studies.

 

Publication metrics (from Scopus):

Number of publications –73

Sum of total citations – 3333

Avg citations per item - 45.7

Number of citations last year – 299

H-index – 33

 

Current and Past Academic Leadership and Citizenship Roles:

  • Secretary of the British Atherosclerosis Society
  • British Heart Foundation Project Grant Committee (2012-2015)
  • Member of the British Council Research Links Grants Committee (2015-ongoing)
  • Editorial Board Membership (Cardiovascular Research, and Vascular Pharmacology)
  • British Atherosclerosis Society John French Lecturer 2015
  • Member of the European Society of Cardiology Working Group on Pathogenesis of Atherosclerosis
  • Member of the American Heart Association (councils of ATVB, and Basic Cardiovascular Sciences)
  • Co-Director of Research (Cardiovascular) for Bristol Medical School
  • Deputy Head of Research for School of Clinical Sciences
  • External examiner iBSc in Cardiovascular Research University of Sheffield

Biography

Dr Jason Johnson is a British Heart Foundation Senior Research Fellow and leads the Laboratory of Cardiovascular Pathology at the University of Bristol.

He has a long-standing interest in the pathophysiology of numerous cardiovascular pathologies including atherosclerosis, aortic aneurysms, and restenosis. His studies include a marriage of basic science and translational cardiovascular research with the goal of facilitating the development and deployment of novel therapies to combat the aforementioned cardiovascular diseases, alongside the identification of potential biomarkers of disease progression.

Since gaining his PhD in 2005, Dr Johnson’s research has underpinned the dogma that not all matrix metalloproteinases (MMPs) play detrimental roles in atherosclerotic plaque progression. Moreover, he has aided the identification of a macrophage phenotype (under the control of GM-CSF) which is characterised by high MMP-12 and MMP-14 protein expression alongside low TIMP-3 levels. Further work has also identified a novel node of microRNA regulation within GM-CSF macrophages, highlighting several potential new therapeutic avenues, including miR-181b inhibition and the selective inhibition of MMP-12. Collectively, these studies have made a major contribution to understanding the role of matrix metalloproteinases and macrophage heterogeneity in atherosclerotic plaque progression. Supporting studies in human aneurysm samples and pertinent pre-clinical in vivo models has reaffirmed the notion that the proteolytic profile of macrophage subsets predicts aneurysm development and progression. These findings are now being tested in a novel ex vivo human model of aneurysm that will hopefully supplant the requirement for animal studies.

 

Publication metrics (from Scopus):

Number of publications –73

Sum of total citations – 3333

Avg citations per item - 45.7

Number of citations last year – 299

H-index – 33

 

Current and Past Academic Leadership and Citizenship Roles:

  • Secretary of the British Atherosclerosis Society
  • British Heart Foundation Project Grant Committee (2012-2015)
  • Member of the British Council Research Links Grants Committee (2015-ongoing)
  • Editorial Board Membership (Cardiovascular Research, and Vascular Pharmacology)
  • British Atherosclerosis Society John French Lecturer 2015
  • Member of the European Society of Cardiology Working Group on Pathogenesis of Atherosclerosis
  • Member of the American Heart Association (councils of ATVB, and Basic Cardiovascular Sciences)
  • Co-Director of Research (Cardiovascular) for Bristol Medical School
  • Deputy Head of Research for School of Clinical Sciences
  • External examiner iBSc in Cardiovascular Research University of Sheffield

Expertise

My research focuses on atherosclerosis ? the build up of fatty material on the lining of arteries to form ?plaques? that can partially block the artery and reduce blood flow. Heart attacks and strokes are primarily caused by cracking of these plaques. Exactly what causes the plaques to rupture is not known, and forms the basis of my Fellowship. The fatty material forming the plaque (blockage) consists of different types of cell, and one type of cell, macrophages, may contribute not only to plaque formation, but also to their cracking. The macrophages exist in several forms that are both good and bad with respect to plaque formation and cracking. Bad macrophages have an increased capacity to grow and divide into more cells, increasing the size of the plaque, but may also trigger death of smooth muscle cells that normally stabilise plaques. The bad macrophages ?destabilise? the plaques, and promote cracking.

  • atherosclerosis
  • Memberships

    Organisations

    Bristol Medical School (THS)

    Other sites

    Academic staff

    Recent publications

    View complete publications list in the University of Bristol publications system

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