Dr Heledd Jarosz-Griffiths
- Position: Postdoctoral Research Assistant
- Areas of expertise: Cell Biology; Cell signalling; Alzheimer's disease; Cystic Fibrosis; Immunology
- Email: H.H.Griffiths@leeds.ac.uk
- Location: 6.11 Wellcome Trust Brenner Building
- Website: LinkedIn | Researchgate | ORCID
I obtained my Bachelor of Science degree in Biochemistry with Medical Biochemistry from University of Leeds in 2005, which included an industrial placement year at AstraZeneca, Alderley Park. In 2009 I completed a PhD in Biochemistry at the University of Leeds which was CASE funded by GlaxoSmithKlein, Stevenage. The focus of my PhD research and subsequent postdoctoral appointments at the University of Leeds between 2009-2014 and then at the University of Manchester between 2014-2017 was on molecular mechanisms of Alzheimer’s disease.
I joined the University of Leeds (Oct 2017 - present) as postdoctoral research assistant in the Leeds Institute of Rheumatic and Musculoskeletal Medicine (LIRMM). My research is funded by Cystic Fibrosis Trust Strategic Research Centre (SRC) under the supervision of Prof. Michael McDermott and Prof. Daniel Peckham, in a project called 'Targeting joint disease in cystic fibrosis (CF): identifying therapeutic targets in CF arthropathy'.
Cystic Fibrosis (CF), the most common genetic condition in the UK, is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. CF is a multisystem disease characterized by chronic bronchial infection and progressive lung disease, but it may affect most organs; recent data from the Leeds care record indicate that >20% of patients have a history of CF associated arthritis (CFAA). Our investigations have established that hyper-inflammation is an important contributor to CF disease progression. We have established that chronic activation of the NLRP3 inflammasome is caused by dysregulation of the Epithelial sodium channel (ENaC) as a result of a disruption in ionic balance caused by CFTR misfolding. My research aims to develop a better understanding of the underlying processes of the persistent inflammation and tissue damage which is characteristic of CFAA, and establish whether current small molecule therapies used to correct CFTR function are able to reduce hyper-inflammation in CF.
- PhD Biochemistry
- BSc (Hons) Biochemistry with Medical Biochemistry (Industry)
- Biochemical Society
- British Society for Immunology (BSI)
- European Cystic Fibrosis Society (ECFS)
Research groups and institutes
- Leeds Institute of Rheumatic and Musculoskeletal Medicine
- Inflammatory Musculoskeletal