Dr Ravi Parhar
Postdoctoral Research Fellow
- Centre for Inflammation Research
- Institute for Regeneration and Repair
- University of Edinburgh
Contact details
- Email: rparhar@ed.ac.uk
Address
- Street
-
4-5 Little France Dr
IRR South
Edinburgh BioQuarter - City
- Edinburgh
- Post code
- EH16 4UU
Background
Ravi graduated from Imperial College London (2021, 1st Class honours). During his studies he secured a placement year position at the National Cancer Institute, National Institutes of Health (Bethesda, USA). He then moved north of the border to pursue a PhD under the guidance of Prof Prakash Ramachandran, Prof Neil Henderson and Prof Thomas Otto (Glasgow), where his project involved fate-mapping scar-associated macrophages (SAMs) during progressive and regressive liver fibrosis. In his current post-doctoral position, co-led by Prof Fiona Oakley (University of Newcastle), Ravi is assessing the role of PFKFB3 in liver fibrosis.
Imperial College London - Graduated 2021
University of Edinburgh (PhD) - Graduated 2026
Research summary
Liver biology
Macrophages
MASH
Current research interests
Assessing the role of PFKFB3 in liver fibrosis. PFKFB3 is a metabolic regulator which enhances cellular glucose utilisation to support biological activity - it is shown to be upregulated in chronic liver disease (CLD) and metabolic dysfunction-associated steatohepatitis (MASH). In CLD, increased PFKFB3 activity in hepatocytes promotes the release of inflammatory and pro-fibrotic mediators, with these effects further amplified by macrophages. This suggests that PFKFB3-dependent signalling between hepatocytes, macrophages, and myofibroblasts establishes pro-fibrogenic cellular crosstalk which drives liver fibrosis. We hypothesise that inhibiting PFKFB3 will restore metabolic balance within these cell populations in MASH and thereby limit fibrosis progression. I aim to assess whether pharmacological inhibition of PFKFB3 in human liver slices and pre-clinical MASH models reduces steatosis, inflammation, and fibrosis. I will investigate how PFKFB3 regulates hepatocyte, macrophage, and scar-forming cell biology using cell-specific genetic deletion models, to better define its role in disease progression. Finally, I aim to determine whether targeting PFKFB3 can prevent progression from MASH to MASH-associated hepatocellular carcinoma (MASH-HCC) and whether PFKFB3 inhibitors, alone or in combination with immunotherapy, can suppress tumour growth in established MASH-HCC.Affiliated research centres
Current project grants
UKRI526 - Cell-specific Functions for PFKFB3 in Metabolic Liver Disease. £1,292,521. Jun 25 - Jun 28.