About the Project
We are seeking an enthusiastic candidate to join a fully funded PhD studentship at the Centre for the Cellular Microenvironment (CeMi) at the University of Glasgow, within the theme of Biomaterials for Tissue Engineering and Human Disease Modelling.
The CeMi is a unique multidisciplinary research environment that brings together researchers from the School of Molecular Biosciences and the School of Engineering. Our research is focussed on understanding the interactions between materials, proteins and cells to engineer and control cell behaviour. More about our research can be found at: https://glasgow.thecemi.org/
This studentship is supported by the MAINSTREAM Hub, a UKRI EPSRC-funded collaboration between the Universities of Glasgow, Strathclyde and Nottingham and the NHS, focused on mechanobiology-driven manufacturing of cells and tissues for regenerative medicine. More about MAINSTREAM's research can be found at: https://www.mainstream-hub.org/our-research/.
Statin-associated muscle symptoms (SAMS) are the leading cause of non-adherence to statin therapy, significantly increasing patients' risk of heart attacks and strokes. The underlying mechanisms are unclear, complicating diagnosis and treatment. This project addresses the knowledge gap by testing the novel hypothesis that SAMS result from the disruption of physical and functional interactions between the endoplasmic reticulum (ER) and mitochondria in skeletal muscle. We aim to characterise how statin exposure disrupts these inter-organelle contact sites, leading to calcium dysregulation, oxidative stress, and muscle weakness, using advanced 3D engineered human muscle tissues. The expected outcome is a precise mechanistic understanding that will identify novel therapeutic targets to prevent SAMS, ultimately improving patient adherence to life-saving medications and reducing cardiovascular morbidity and mortality.
Statins are a cornerstone of preventative cardiovascular medicine. However, SAMS are a major limitation to their effectiveness. Current research has identified isolated issues with mitochondria (CoQ10 depletion, energy loss) and the ER (calcium leaks), but our approach is unique in focusing on their interaction. Understanding this inter-organelle crosstalk provides a unifying, novel mechanism that promises targeted therapeutic development. This fills a critical knowledge gap and moves the field beyond empirical solutions like CoQ10 supplementation, which has shown inconsistent results.
This PhD project will characterise statin-induced structural changes in ER-mitochondrial contact sites in human myotubes using super-resolution and electron microscopy and quantify calcium transfer kinetics between the ER and mitochondria using live-cell imaging with targeted GCaMP calcium sensors in control versus statin-treated bioartificial muscles. We will investigate the link between this organelle-axis disruption and downstream muscle pathology by measuring reactive oxygen species production, integrated stress response markers, and protein degradation pathways, and evaluate novel therapeutic targets, such as RyR1 stabilisers and mitochondria-targeted antioxidants, in both the 3D human muscle tissue model and a pre-clinical rat model of statin myopathy.
SAMS affect up to 29% of patients and are the primary reason for prematurely discontinuing life-saving statin medications, so this research has substantial scientific, clinical, and economic impact. It will provide the first detailed characterisation of how statins disrupt MERCs, moving beyond existing theories of isolated organelle dysfunction, and will establish a highly biomimetic 3D muscle tissue platform for more predictive pre-clinical drug screening. Clinically, a clearer mechanistic understanding will help distinguish true statin myopathy from the nocebo effect and support the development of adjunct therapies that protect muscle without compromising cholesterol-lowering efficacy, ultimately reducing preventable cardiovascular events and improving quality of life for the millions of people who rely on statin treatment.
How to Apply: Please refer to the following website for details on how to apply: http://www.gla.ac.uk/research/opportunities/howtoapplyforaresearchdegree/.
Funding Notes
Funding covers a full UKRI stipend and tuition fees for UK and EU (resident) applicants, at the UKRI rate of £21,805 for 2026/27.
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