Dr Sofia Ahola

Supervisor Details

Contact Details

Department of Metabolism and Systems Science, University of Birmingham

Scientific Background

Research Interests

I’m fascinated by how mitochondria keep cells alive and what happens when they don’t. My group studies the molecular mechanisms of mitochondrial diseases and their tissue-specific “fingerprints.” We focus on stress responses and metabolic rewiring that follow mitochondrial dysfunction, and on what tips cells into distinct death pathways, especially ferroptosis. Although many mitochondrial disorders stem from primary defects in oxidative phosphorylation (OXPHOS), the same mutation can cause very different symptoms in different organs and people. Unpicking this complexity is my core motivation. We combine tissue-specific cell culture systems, iPSC-derived models, and in vivo approaches with metabolomics, proteomics, and advanced imaging to map how mitochondrial stress signalling protects, or fails, and how that shapes disease. Our long-term goal is to convert mechanistic insight into new therapeutic strategies.

Scientific Inspiration

What drives me is curiosity: the feeling that mitochondria are holding on to secrets that, once revealed, will change how we treat patients. Mitochondrial diseases are biologically intricate and clinically diverse; that mystery energises me. I’m also a scientific artist, and I bring that visual mindset into the lab, using imaging to see processes as they unfold, and drawing to clarify ideas and communicate them clearly (some of my science-inspired art is shown in www.sofiaahola.com). I love working with students who want to ask bold questions, learn powerful methods, and turn uncertainty into discovery. If you enjoy connecting biochemistry, cell biology, metabolism and imaging, and you like the idea of solving puzzles that matter to patients, then you’ll fit right in.

Supervision Style

In three words or phrases: My supervision style is supportive and encouraging, while giving students ownership of their projects and fostering independence. I aim to be goal-oriented and structured without micromanaging, ensuring steady progress while allowing room for creativity. I value inclusivity and collaboration, and strive to create an environment where students feel confident, motivated, and empowered to grow as researchers.

Provision of Training

I prefer to take responsibility for your technical training at first, leading to more independence later.

Progression Monitoring and Management

I set clear expectations for progression and review them regularly, usually on a weekly or monthly basis, while remaining flexible to adjust according to the student’s needs and project phase. I am available for more frequent support when required, especially at the beginning, and always address challenges collaboratively by agreeing on a plan of action together.

Communication

I like to keep communication within normal working hours to support a healthy work–life balance, but I’m happy to be flexible if needed. I value open and supportive communication and want students to feel comfortable reaching out at any time.

Meetings

PhD Students can expect scheduled meetings with me at least once per month. These meetings will be face-to-face. I am usually contactable for an instant response on every working day.

Work Patterns

Certain tasks in my lab need to occur at set times, and students need to be able to commit to a rota/timetable shared with other members of the team.

Notice Period for Feedback

I need at least 2 weeks' notice to provide feedback on written work of up to 5,000 words.

MIBTP Project Details

Primary supervisor for:

Fuel, Iron, and Fire: Mitochondrial Iron Metabolism in Ageing

See the PhD Opportunities section to see if this project is currently open for applications via MIBTP.

Please Note: The main page lists projects via BBSRC Research Theme(s) quoted and then relevant Topic(s).

Fuel, Iron, and Fire: Mitochondrial Iron Metabolism in Ageing

Secondary Supervisor(s): Prof Daniel Tennant

University of Registration: University of Birmingham

BBSRC Research Themes:

Integrated Understanding of Health (Ageing, Diet and Health)

Project Outline

Skeletal muscle undergoes progressive loss of mass and function during ageing, a process termed sarcopenia. This decline arises from reduced myogenesis and degeneration of existing fibres, leading to frailty and an increase in metabolic disease. The hallmarks of ageing propose that ageing is driven by the decline of mitochondrial function and accumulation of oxidative damage. Mitochondria act as metabolic hubs, hosting the oxidative phosphorylation and iron–sulfur cluster (Fe–Sc) biogenesis. Fe–Sc are essential cofactors for respiration, DNA maintenance and redox homeostasis. Their synthesis requires cysteine as a sulphur donor, linking mitochondrial iron and thiol handling to antioxidant systems. Disruption of Fe–S biogenesis leads to iron misregulation, impaired respiration and excess oxidation. One outcome of disturbed iron–thiol metabolism is vulnerability to ferroptosis, a cell death driven by iron-dependent lipid peroxidation[1]. Ferroptotic susceptibility depends on iron and sulfite handling as well as lipid composition and selenoprotein peroxidases. Thus, dietary factors such as selenium intake and lipids, together with mitochondrial Fe–S cluster assembly, may act as upstream regulators of ferroptosis sensitivity in ageing muscle.

When mitochondria decline, protective stress responses are activated. The oxidative stress response mediated by Nrf2 can upregulate cysteine and Fe metabolism and antioxidant defences. Previous work has shown that these pathways mitigate ferroptosis in mitochondrial cardiomyopathy[2]. This project will investigate how mitochondrial Fe–S metabolism and cysteine handling intersect with ferroptosis in ageing muscle.

Objectives

1. Characterise mitochondrial Fe–S biogenesis and cysteine metabolism in aged myoblasts

2. Determine ferroptosis sensitivity in aged myoblasts and test the influence of selenium and lipids

3. Evaluate Nrf2 activation and ferroptosis in aged mouse skeletal muscle

1. Ahola et al.TCB2024 2. Ahola et al.CellMet2022

APPLY HERE