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Full NameDr Katarzyna Goljanek-Whysall

Department:Physiology

Organisation:National University of Ireland Galway

Webpage:wixsite.com

Email Address:Email hidden; Javascript is required.

Research Fields
  • genetics, genomics and molecular biology
  • cell and developmental biology/regenerative medicine
  • physiology and non-communicable disease
  • cancer/oncology
  • Other
Other Research Fields:

microRNAs, epigenetic, non-coding RNAs

Postgrad Medical Specialties
  • Medicine
  • Surgery
  • Anaesthetics
  • General Practice
  • Pathology
  • Sports and Exercise Medicine
Medical Subspecialties
  • Endocrinology
  • Geriatric Medicine
  • Health Informatics
  • Oncology
  • Physiology
  • Rheumatology
My Work

My research group is interested in the role of epigenetic mechanisms in musculoskeletal tissues homeostasis, specifically the aspects related to decline of muscle, cartilage and tendon function and regenerative potential. We use in vitro and in vivo model systems to study the functional aspects of dysregulation of epigenetic mechanisms during ageing and disease. Our aim is to establish novel biomarkers and therapeutics against age-related disorders of the musculoskeletal tissues. More recently, we have been investigating microRNAs as potential therapeutic for muscle wasting during cancer cachexia and amyotrophic lateral sclerosis.
Our research is funded by BBSRC, Dunhill Medical Trust, Orthopaedic Research UK, CIMA, IRC.

Selected publications:

- Goljanek-Whysall K., Sweetman D., Abu-Elmagd M., Chapnik E., Dalmay T., Hornstein E., Munsterberg A.; MicroRNA regulation of the paired-box transcription factor Pax3 confers robustness to developmental timing of myogenesis; Proc Natl Acad Sci USA, 2011.
- Goljanek-Whysall K., Pais H., Rathjen T., Sweetman D., Dalmay T., Munsterberg A.,; Regulation of multiple target genes by miR-1/miR-206 is pivotal for C2C12 myoblast differentiation; Journal of Cell Science, 2012.
Goljanek-Whysall K, Mok G., Al Fahad A., Kennerley N., Wheeler G., Munsterberg A.; myomiR-dependent switching of BAF60 variant incorporation into Brg1 chromatin remodeling complexes during embryo myogenesis, Development, 2014.
- Soriano-Arroquia A., McArdle A., Molloy A., Goljanek-Whysall K; Age-related changes in miR-143:Igfbp5 interactions affect muscle regeneration, Aging Cell, 2016.
- Soriano-Arroquia A., House L., Tregilgas L., Canty-Laird E., Goljanek-Whysall K.; The functional consequences of age-related changes in microRNA expression in skeletal muscle; Biogerontology, 2016.
- Goljanek-Whysall K, Proctor C; Using computer simulation models to select the most promising microRNA therapeutics against sarcopenia, Scientific Reports, 2017
- Sannicandro A, Sorriano-Arroquia A, Goljanek-Whysall K; micro(RNA)-managing muscle wasting; Journal of Applied Physiology, 2019.
- Shorter E., Sannicancdro T., Poulet B., Goljanek-Whysall K.; Skeletal muscle wasting and it relationship with osteoarthritis: a mini review of mechanisms and current interventions; Curr Rheumatol Rep; 2019.
- Sannicandro AJ, McDonagh B, Goljanek-Whysall K, MicroRNAs as potential therapeutic targets for muscle wasting during cáncer cachexia; Curr Opin Clin Nutr Metab Care, 2020.
- Goljanek-Whysall K, Chinda C, McCormick R, Soriano A, McDonagh B; Age-related changes in miR-181 expression regulate mitophagy in skeletal muscle. BiorXiv, 2019, Aging Cell, in press.

Potential Projects

microRNAs as potential therapeutics for muscle wasting in ageing and disease

Irreversible muscle loss due to ageing (sarcopenia) or disease such as cancer (cachexia) or critical illness such as sepsis, is a major socio-economic and healthcare burden that will increase with our ageing population and in the light of the current health care challenges. Muscle loss leads to frailty, hospitalisation and is prognostic of morbidity and mortality. Patients, e.g. cancer or critically ill, with lower muscle mass show worse recovery and even response to the therapy. Despite progress in understanding muscle loss, no effective therapies exist. Exercise can delay, but not reverse, muscle loss in a small group of patients.

Based on our work demonstrating that during ageing and disease, microRNAs levels are altered and microRNAs can be modified to regulate alternative set of genes and inhibiting pathogenic miRs improves muscle size and strength in vivo, we hypothesise that imiR-based approcahes can provide an alternative, effective therapy against muscle loss.

The project will use a combination of discovery-driven omics and bioinformatics to characterise changes in microRNAs during muscle wasting. Functional studies in models of muscle loss will validate the crucial role of miRs in muscle wasting and provide evidence for the use of oxi-miR inhibitors to improve muscle mass and strength.