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Full NameProfessor Paul McLoughlin

Department:Conway Institute

Organisation:University College Dublin

Webpage:people.ucd.ie

Email Address:Email hidden; Javascript is required.

Research Fields

  • physiology and non-communicable disease
  • bioengineering/medical devices

Postgrad Medical Specialties

  • Medicine
  • Surgery
  • Anaesthetics
  • Paediatrics
  • Pathology

Medical Subspecialties

  • Cardiology
  • Physiology
  • Respiratory Medicine
  • Vascular Medicine

My Work

Our research explores key mechanisms in the development and progression of chronic hypoxic lung diseases characterized by inflammation and pulmonary fibrosis.

We have shown that a specific family of proteins, known as the bone morphogenetic antagonists, plays a major role in the development of hypoxic pulmonary hypertension (WHO Group 3 PH) and more recently we have shown that these proteins also contribute to the development of idiopathic pulmonary fibrosis (1-3). We are currently exploring the molecular pathways through which one of the most important members of this family (gremlin 1) acts (4).

A second research focus is altered endothelial barrier function and the development of pulmonary oedema in diseases such as ARDS and systemic sepsis. Interestingly, this work also has the potential to improve the supply of donor lungs for transplant by enhancing ex vivo machine perfusion strategies (5).

1. Cahill et al. Circulation. 2012 Feb 21;125(7):920-30. PMID: 22247494
2. Murphy et al. Am J Pathol. 2016 Mar;186(3):600-15. PMID: 26765958
3. Rowan et al. Lancet Respir Med. 2016 Mar;4(3):225-36. PMID: 26895650
4. Rowan et al. Pulm Circ. 2018 Oct 4:2045894018807205. doi: 10.1177/2045894018807205. PMID: 30284507
5. Rowan et al. Am J Physiol Lung Cell Mol Physiol. 2018 Oct 1;315(4):L476-L484. PMID: 29792349

Potential Projects

Project 1. Regulation of macrophage function by the bone morphogenetic proteins and their antagonists in pulmonary fibrosis.
Macrophages recruited to the lung as monocytes are central to the pathogenesis of pulmonary fibrosis. In the lung, the monocytes differentiate into macrophages, become alternatively polarised (M2-like) and produce pro-fibrotic mediators that cause pulmonary fibrosis in animal models. Recent work in our laboratory in pre-clinical cellular and animal models has shown that the bone morphogenetic proteins and their antagonists act to control this process. This translational project will examine the role of the BMP signalling axis in regulating the function of macrophages derived from healthy human monocytes and the role of these signaling pathways in blood monocyte-derived macrophages from patients with pulmonary fibrosis.

Project 2. The role of blood viscosity in maintaining normal endothelial barrier function and preventing oedema in the pulmonary circulation: implications for lung transplantation programmes.
We have recently shown for the first time that the use of macromolecules to increase the viscosity of artificial perfusion solutions so that it is similar to that of normal blood improves endothelial barrier function in the lung and protects against oedema formation. However, the cellular and molecular mechanisms of this protective action are currently unknown. This project will explore the mechanisms by which increased viscosity improves endothelial barrier function using pre-clinical isolated lung models, both rodent and porcine. Based on the underlying mechanisms, high viscosity perfusion solutions will be optimized and examined in human lungs offered for donation but following assessment are found to be unsuitable.