Sara Wickström awarded the Körber Prize 2026

Text: Linda Geddes

Sara Wickström is a pioneer in the mechanobiology of the cell nucleus. The Finnish physician and cell biologist has uncovered how physical forces such as stretch, compression and tension are sensed by cells and translated into molecular signals that control gene activity. Her research shows how these forces reshape the genetic information packaged within the chromatin of the cell nucleus and determine how cells develop, regenerate or respond to disease. These insights open new avenues for treating cancer, organ scarring and other age-related conditions. With the Körber Prize funds, Wickström intends to investigate whether cells develop a ‘memory’ of injuries and mechanical stresses, and whether this can be influenced in the context of future therapies.

When Sara Wickström first peered down a microscope at a cell’s internal skeleton, she was struck by its beauty. Long filaments criss-crossed the cell’s interior, terminating in bright, blob-like adhesions at its outer edges, where the cell latched onto its surroundings. Chemically stained with fluorescent dyes and antibodies, they glowed neon against the darkness, revealing a secret world whose significance was only beginning to become clear.

At the time, textbooks often likened the fibres and connections of this “cytoskeleton” to the beams and cables of a building: an internal scaffold that helped cells maintain their shape, move through tissues and organise the transport of molecules within the cell. But that view was beginning to change. Scientists were starting to realise that the cytoskeleton did far more than provide structure. Linked to the outside world through anchor points called focal adhesions, and powered by tiny molecular motors fuelled by ATP, the cytoskeleton also enabled cells to physically sense their environment – robing stiffness, tension and compression, and responding accordingly.

Over the next two decades, Wickström would help reveal just how profound those hidden physical forces really are. Her work showed that external mechanical stresses triggered by a cell’s environment can reach all the way into the nucleus, reorganising the packaging of DNA and altering gene expression itself. Cells, it turns out, do not only respond to genetic instructions and chemical signals. They also continuously interpret the physical environments they inhabit, sensing, adapting to, and sometimes even remembering them.

“Through her transformative work, which has shaped modern cell biology, Wickström has redefined the understanding of the integration of mechanical and biochemical information within living tissues,” says Edvard Moser, Chairman of the Körber Prize Search Committee Life Sciences.

Her discoveries are now reshaping how scientists think about stem cells, regeneration, cancer and ageing, while opening new possibilities for diagnosing and treating diseases linked to abnormal tissue mechanics, including fibrosis – a pathological overgrowth of scar tissue that progressively impairs organ function and contributes to many age-related diseases.

Using the Körber Prize funding, Wickström plans to investigate why these abnormal tissue states persist and whether it may be possible to reprogramme them, promoting healthy tissue function instead of chronic scarring.

Learning through observation

Even as a child growing up in Finland, Wickström was fascinated by the forces that govern everyday phenomena. “I liked, and still like, observing things,” she says. She was initially drawn to the concrete worlds of physics and mathematics. Biology was barely on her radar. Although she once wrote on a school careers questionnaire that she wanted to become “a professor”, she struggled to imagine herself as a physicist. “I somehow thought that I’m not smart enough,” she recalls. “You have these impressions of geniuses in their chambers.”

Nevertheless, the world of science and experimentation strongly appealed to her, even if she had little sense of what a life in research might actually look like. Her mother, a gym teacher and student counsellor, suggested a practical solution: a combined medicine and PhD programme at the University of Helsinki that would expose her to research, yet also equip her with a profession, should she decide science wasn’t for her.

With hindsight, it proved an inspired choice: medicine grounded Wickström in the realities of the body and disease, while her longstanding fascination with physics would eventually shape her approach to studying living tissue.

It was during a summer rotation in a cell biology laboratory that she encountered the kind of science that finally clicked with her.

She was captivated, not only by the cells themselves but also by the process of discovery – formulating hypotheses, designing experiments, optimising conditions and gradually building understanding. “I immediately thought: that’s great – that’s my thing. Let’s study cells.”

After completing her medical degree and spending a year working as a general practitioner, Wickström returned to academia to pursue a PhD. She joined the laboratory of Jorma Keski-Oja at the University of Helsinki, where researchers were probing the complex interactions between cells and the extracellular matrix – the dense meshwork of proteins that surrounds cells.

Historically, scientists had viewed the extracellular matrix as passive scaffolding, something that provided tissues with structural support but little else. But Wickström entered the field at a time when researchers were starting to appreciate how dynamic the relationship between cells and their environment could be. Cells, it turns out, not only build and remodel the matrix around them, but they continuously interact with it – pulling on it, sensing it and responding to the biochemical and mechanical cues it provides.

Wickström’s own PhD project focused on endostatin, a fragment of collagen that had generated enormous excitement as a potential anti-cancer drug because of its apparent ability to block the growth of blood vessels feeding tumours. Using cultured endothelial cells, she investigated how endostatin altered cell adhesion and the actin cytoskeleton – the dynamic network of protein filaments that helps cells maintain their shape, generate force and physically interact with their surroundings.

Wickström had to take responsibility for many practical aspects of the research herself – formulating a project from scratch, designing experiments, writing papers and corresponding with journals. The experience also reinforced her growing fascination with how cells sense and respond to the environment around them.

For her postdoctoral work, she joined the laboratory of Reinhard Fässler at the Max Planck Institute of Biochemistry in Martinsried, Germany, a world-leading centre for the study of cell adhesion. There, using mouse models, Wickström began investigating how cells co-ordinate their behaviour within the dynamic architecture of the skin.

Her focus was on integrins, the molecular adhesion complexes that allow cells to physically attach to the extracellular matrix around them. More than simple anchors, integrins also relay information about the physical properties of a cell’s surroundings.

The skin’s outer layer, the epidermis, proved an especially powerful system in which to study these questions. Forming a critical barrier between the body and the outside world, the epidermis is constantly renewing itself. Stem cells attached to a thin underlying basement membrane continuously divide, while older cells differentiate and migrate towards the skin’s surface, where they are eventually shed. Beneath the epidermis lies the dermis, a deeper layer of connective tissue, rich in extracellular matrix.

Besides self-renewal, the epidermis is continually subjected to stretching, compression and friction, yet it somehow maintains its highly ordered structure. Wickström became fascinated by how it balances constant renewal with such remarkable mechanical resilience.

An accidental breakthrough

By 2010, Wickström was leading her own research group at the Max Planck Institute for Biology of Ageing in Cologne, where her laboratory was investigating how mechanical forces influence skin stem cells. It was an exciting time for biology, which was undergoing two parallel revolutions. The first concerned mechanics. Researchers increasingly appreciated that cells were not passive entities shaped solely by genes and chemical signals. Through focal adhesions and the cytoskeleton, cells could physically probe their surroundings, detect stiffness and tension, and adjust their behaviour accordingly.

For Wickström, the epidermis offered a vivid example of this principle in action. The skin on the soles of our feet is thick and heavily reinforced to withstand constant compressive pressure. Skin around the elbows wrinkles into folds that tolerate continual stretching and folding, while eyelid skin remains thin and delicate. Yet all are built from essentially the same kinds of cells. “It became clear that somehow forces must be important,” Wickström recalls.

At the same time, another revolution was unfolding inside the nucleus. Scientists were discovering that cellular identity depends not only on DNA sequence but also on how DNA is packaged. Chemical or “epigenetic” modifications to chromatin – the complex of DNA and histone proteins that bundles DNA up within the nucleus – help determine which genes are switched on or silenced, allowing stem cells to adopt specialised identities.

Yet despite growing excitement in both fields, mechanics and epigenetics remained largely separate worlds. The question Wickström’s laboratory began to tackle was whether physical forces acting on tissues could somehow reach all the way into the nucleus and reorganise chromatin – providing a direct bridge between a cell’s physical environment and gene expression.

The researchers were particularly interested in whether stretching forces in skin stem cells could act as a growth signal. So they grew skin stem cells on flexible membranes that could be mechanically stretched, mimicking some of the physical forces experienced by skin in the body. They then used RNA sequencing to analyse how gene activity changed inside the cells.

The team expected to find specific growth-related genes switching on or off in response to stretching. Instead, they encountered something far stranger. “Somehow thousands of genes were downregulated,” says Wickström. “It was very unusual.”

Rather than pointing to a conventional signalling pathway, the results suggested that mechanical force was triggering a much broader reorganisation of gene activity – one that Wickström suspected might involve epigenetic changes.

Epigenetics was still an emerging field, and Wickström had little formal background in it. “I thought: this is risky,” she says. “But if it’s true, then it’s something really, really new.”

Further analysis revealed that many of the silenced genes carried the molecular signature of a major epigenetic regulator known as Polycomb Repressive Complex 2 (PRC2), which helps switch genes off by chemically modifying chromatin. Wickström’s group began tracing how physical force applied at the cell surface might influence this system. Using microscopy, molecular biology and biomechanical experiments, they showed that stretching reorganised the cytoskeleton surrounding the nucleus and altered the architecture of chromatin inside it, reshaping how DNA was packaged and which genes could be accessed.

The findings, published in Nature Cell Biology in 2016, helped provide one of the clearest demonstrations yet that mechanical forces are not merely external stresses acting on tissues but fundamental regulators of cellular identity.

“It gave rise to an entirely new field at the interface of molecular and mechanical control of cell fate dynamics,” says George Cotsarelis, Milton B. Hartzell Professor at the Perelman School of Medicine in Philadelphia, US.

How cells remember past environments

The implications extended far beyond skin biology. If mechanical forces could reshape chromatin, then cells might also retain molecular traces of past physical environments – a form of epigenetic memory that could influence ageing, regeneration and disease long after the original forces had disappeared.

For Boris Hinz, Professor of tissue repair and regenerative medicine at the University of Toronto and Keenan Chair in Fibrosis Research at Unity Health Toronto, this was one of the discoveries that helped fundamentally reshape the field. “By shifting the dogma of how gene transcription is regulated in response to cells’ mechanical environment, Dr Wickström’s findings have had a profound impact on our understanding of fundamental cell biological processes,” he says.

Mechanical signals are now understood to influence biology across almost every stage of life. During embryonic development, physical forces help guide cells towards specialised identities as tissues form and fold into shape. In adult organisms, the conversion of physical forces into biochemical responses enables tissues to adapt to their environment: heart muscle cells respond to the strain of contraction, endothelial cells lining blood vessels sense changing blood flow, while connective tissue cells continuously remodel bone, cartilage and tendons in response to mechanical load.

Following the 2016 study, Wickström’s laboratory continued to probe how forces reshape cellular identity across tissues and timescales. A 2020 study published in Cell revealed that chromatin does more than regulate genes: it also helps to physically protect the genome from mechanical stress. When skin cells were stretched, their nuclei deformed in response. To prevent DNA damage, the cells temporarily loosened tightly packed regions of chromatin, softening the nucleus and allowing it to better absorb the stress.

More recent work has shown that physical crowding, osmotic pressure and tissue stiffness can also influence what stem cells differentiate into by altering how tightly DNA is packaged within the nucleus. Increasingly, the nucleus is viewed not simply as a passive container for genetic material, but as a structure that continuously interprets and responds to the physical world around it.

From discovery to translation

For Wickström, some key remaining questions are the extent to which these mechanisms are utilised in cells’ daily lives, under what circumstances, and whether they could be targeted to help patients with diseases associated with abnormal tissue mechanics. In diseases such as cardiac or pulmonary fibrosis and cancer, for instance, tissues often become abnormally stiff, and cells exposed to these environments may become trapped in a negative spiral, maintained by the epigenetic and chromatin changes that Wickström’s work has helped to reveal. “Understanding the molecular basis could enable strategies to prevent cells from entering or remaining in such disease states and to restore normal function,” says Hinz.

Using the funding associated with the Körber Prize, Wickström plans to investigate how tissues remember changes in their structure. Return to normal tissue function after injury requires damaged tissue to rebuild its normal structure and mechanical properties. Yet healing in humans and other large mammals often leaves scars instead. Over time, these dense, stiffened regions of extracellular matrix can develop into a chronic form of pathological scarring known as fibrosis.

“Fibrosis is an end-stage condition of many deadly diseases, including cancer,” says Hinz. Fibrotic diseases can also affect the lungs, heart, liver and kidneys, impairing organ function and quality of life, and are estimated to contribute to a substantial proportion of deaths worldwide. Yet scientists still do not fully understand why some tissues successfully resolve injury while others become trapped in chronic cycles of inflammation and scarring.

Wickström believes mechanics may provide part of the answer. “Fibrosis fundamentally alters the physical environment surrounding cells, making tissues stiffer and changing how forces are transmitted through them,” she says. Her hypothesis is that cells exposed to these abnormal mechanical environments may acquire lasting epigenetic memories encoded within chromatin.

By tracking individual cells as they are exposed to repeated mechanical stress in cell culture, or during the healing process in tissues, and observing how stiffness and mechanical stress alter chromatin and gene regulation, she hopes to better understand how injury can lock cells into harmful, disease-maintaining states, and whether this could eventually be reversed.

These findings could help to reduce scarring after severe burns or aid in the closure of non-healing wounds in elderly and diabetic patients.

Cheng-Ming Chuong, Professor of Pathology at the University of Southern California in Los Angeles, said: “These cutting-edge approaches have the potential to significantly advance our understanding of mechanobiology and to uncover new strategies for controlling fibrosis and regenerative responses.”

Another long-term ambition of Wickström’s research is to identify mechanical and chromatin-based biomarkers that could help detect cancers earlier or predict how tissues will respond to injury and ageing.

“Cancer starts from mutations, so it’s something that happens inside cells, but it’s inherently still associated with disruption of this healthy tissue architecture,” Wickström says.

Healthy tissues are highly organised, with different cell types continuously communicating through chemical and mechanical signals. As tumours grow, that organisation breaks down: the extracellular matrix is remodelled, surrounding tissues often stiffen and become inflamed, and the physical environment experienced by cells changes profoundly. “We wanted to understand to what extent this architecture gives us additional biological information that merely analysing the mutations does not,” Wickström says.

Using imaging, molecular markers and computer algorithms, her team has mapped not only cancer cells but also the surrounding tissue environment, including immune cells, connective tissue and other non-cancerous cells reacting to the tumour. Their work suggests that the organisation of these cells, and their relationships to one another, may contain important clues about how aggressive a tumour is likely to be.

To help move these ideas towards clinical application, Wickström, together with two postdoctoral scientists from her laboratory who were excited by the translational potential of this work, founded the diagnostics company MultivisionDx, which applies artificial intelligence and tissue architecture analysis to microscopic images of tumour tissue.

The hidden physics of life

Now Director of the Max Planck Institute for Molecular Biomedicine and Research Director at the University of Helsinki’s Faculty of Medicine, Wickström has long surpassed her childhood dream of becoming a professor. Yet she sees the role as serving two purposes: advancing scientific discovery while also helping to develop the next generation of scientists.

Equally central to her philosophy is multidisciplinary collaboration. In her laboratory, physicists, clinicians, engineers, computational scientists and cell biologists work side by side, combining microscopy, genomics, pathology, biophysics and machine learning. “Often, the hard problems in biology are interdisciplinary, which is why they have remained unresolved,” she says. “And I think this is an exciting moment, because of computation, live imaging and so on, that we finally can address them properly – and I want to be at the forefront of that.”

In many ways, her own career has come full circle: from an early fascination with physics and observation, through medicine and cell biology, back towards physics again – but now inside living tissue.

Despite the scale of her discoveries, Wickström remains strikingly modest about her achievements, describing the discovery linking force to chromatin regulation as “purely serendipitous”.

She repeatedly returns to ideas of patience, curiosity and the gradual accumulation of knowledge. Although she “likes a hypothesis”, she still prefers to observe and to “let the biology teach me”. When recruiting researchers to her laboratory, she is often less interested in prior expertise in tissue mechanics than in the new perspectives people can bring. “We can teach people what we know,” she says. “But when people come with their own expertise, they teach us what they know – and that’s where unique perspectives come from.”

Basic researchers, she says, are often driven by curiosity and fascinated by mechanisms that may eventually illuminate disease, but they may not always be asking the questions most relevant to clinical need. Clinicians, meanwhile, are focused on the immediate realities of helping patients and may not fully appreciate the potential of cutting-edge science to transform medicine. The patient perspective, she believes, is often overlooked altogether.

As part of her Körber Prize outreach programme, Wickström hopes to bring these perspectives together through interdisciplinary public workshops exploring tissue mechanics and scarring. Here, clinicians would teach participants how to physically assess scar tissue by touch, patients would describe how fibrosis affects their daily lives, while scientists and students would demonstrate – using live microscopy and force-measuring tools – how changes in tissue stiffness alter cellular behaviour.

In many ways, this philosophy mirrors the science. Just as cells are continuously shaped by the environments they inhabit, Wickström believes scientific discovery flourishes when different perspectives, disciplines and lived experiences are brought together. “There are so many fantastic advances in science,” she says. “But I don’t think it’s always clear to the general public what science could actually do if we fully leveraged its power.”

Sara Wickström is a Finnish physician-scientist and Director at the Max Planck Institute for Molecular Biomedicine in Münster, Germany, where she leads research into how physical forces shape the behaviour of cells and tissues. She also serves part-time as Research Director at the University of Helsinki’s Faculty of Medicine.

Born in Finland in 1976, Wickström developed an early fascination with physics and mathematics but chose to study medicine through a combined MD-PhD programme at the University of Helsinki. During a laboratory rotation in cell biology, she became captivated by experimental science and the emerging questions surrounding how cells physically interact with their environment.

After qualifying as a doctor in 2001 and spending a year working as a general practitioner, she completed her PhD at the University of Helsinki in 2004.

She then moved to Germany for postdoctoral research at the Max Planck Institute of Biochemistry before establishing her own research group at the Max Planck Institute for Biology of Ageing in 2010. Her laboratory later relocated to Helsinki, where she became a professor of cell and developmental biology in 2021.

Wickström is internationally recognised for pioneering work showing that physical forces acting on cells can reorganise chromatin and alter gene activity, helping to establish the emerging field of mechanobiology. Her discoveries have reshaped scientific understanding of stem cells, tissue regeneration, fibrosis and cancer while opening new possibilities for diagnostics and regenerative medicine.

Her laboratory is highly interdisciplinary, bringing together physicists, clinicians, engineers, computational scientists and biologists to investigate how tissues maintain themselves, respond to injury and become diseased. Current research focuses on mechanochemical signalling, tissue regeneration, fibrosis and cancer progression, with the long-term goal of developing new diagnostic and therapeutic strategies.

Wickström has received numerous honours for her research, including the German Society for Cell Biology’s Binder Innovation Prize in 2017, the A. I. Virtanen Research Prize and the American Society for Cell Biology’s Innovation in Research Award in 2023, and the 2026 Körber European Science Prize. She was elected a member of EMBO in 2020 and named one of Cell Press’s “50 Scientists That Inspire” in 2024.

Alongside her research, Wickström plays an active role in the international scientific community. She serves as Deputy Editor of Science Advances, sits on multiple international advisory boards and grant panels, and has helped to lead interdisciplinary graduate training programmes in Germany and Finland.

Together with collaborators, Wickström also co-founded the diagnostics company MultivisionDx, which uses artificial intelligence and tissue architecture analysis to improve cancer pathology.

Beyond her scientific achievements, Wickström is deeply committed to mentoring young researchers and improving communication between scientists, clinicians and patients. Through her outreach activities, she aims to make the hidden mechanics of living tissue more accessible to the public and to strengthen connections between fundamental biology and clinical medicine.

Professor Werner, as a member of the Körber Prize Search Committee: What distinguishes the selection process from other major scientific awards?

The Körber Prize is unique because it looks beyond past achievements to deliberately invest in the future. We not only honour a single discovery; we also recognise scientists whose groundbreaking work has opened an entire new field. Our goal is to identify researchers with the potential to drive their disciplines in transformative directions.

What makes the process particularly compelling is the two-stage selection. Candidates are nominated by leading institutions across Europe or by members of the scientific committees of the Prize. After a first evaluation of all proposed scientists, a limited number is invited to submit a research proposal. This allows us to evaluate both their track record and their future scientific trajectory. In this sense, the prize isn’t just a recognition of past achievements – it is a catalyst for the next breakthrough.

What defines groundbreaking research in life sciences today – and where do you see the greatest future potential?

Groundbreaking research often emerges at the interface of disciplines. We are moving away from studying individual molecules or pathways in isolation; we aim to understand how different signaling pathways interact within living systems, how this is shaped by environmental cues, and how dysregulation of certain pathways causes disease.

A particularly important research question is how mechanical forces interact with biochemical signals to shape cellular responses. For a long time, the effects of different mechanical forces on cell behaviour were largely overlooked, and mechanistic mechanobiological studies were scarce. This interdisciplinary frontier holds enormous potential. It allows us to leverage Europe’s strengths in fundamental physical and biological sciences to develop innovative regenerative medicine and advanced treatments for various disorders, including cancer and degenerative diseases.

Why is Sara Wickström’s research on mechanical forces and gene regulation so significant for modern cell biology?

Sara Wickström discovered that chromatin architecture and consequently transcription are regulated not only by biochemical signals but also by extrinsic physical forces like stretching and compression. By identifying the nucleus as an autonomous mechanosensor, she pioneered a new field of research. Her work is characterised by remarkable mechanistic depth and high translational potential. It links mechanical signals to tissue morphogenesis and repair, aging, and oncogenesis. This opens new avenues for the development of therapeutic strategies that target mechanosensitive pathways.

Sara Wickström receives the 2026 Körber Prize for her pioneering discoveries on the role of mechanical forces in the regulation of stem cell fate by controlling molecular signaling and epigenetic gene regulation. Through her transformative work, which has shaped modern cell biology, Wickström redefined the understanding of the integration of mechanical and biochemical information within living tissues.

She has uncovered fundamental mechanisms by which cells sense mechanical forces – such as stretch, compression, or shear – and transmit these cues to the nucleus. Wickström demonstrated how these forces remodel chromatin architecture, alter epigenetic states, and regulate access to DNA, thereby directing gene expression and long-term cellular behavior. Among her landmark discoveries is the finding that heterochromatin-driven nuclear softening protects the genome from mechanically-induced damage, revealing a previously unrecognized strategy by which cells preserve genomic integrity. Wickström has shown that mechanical forces, whether arising from the external environment or from internal tissue architecture, guide cell-state decisions during development, regeneration, and disease. Her work has illuminated how mechanical stress – both acute and encoded as epigenetic memory – shapes epithelial dynamics and influences cellular responses in contexts such as tissue repair and tumor progression.

Wickström’s discoveries span scales from molecular regulation to tissue physiology and have opened new avenues for translational research. By identifying mechanosensitive pathways and epigenetic signatures associated with tissue dysfunction, Wickström’s work holds great promise for the identification of prognostic biomarkers and for therapeutic strategies targeting fibrotic and other mechanically driven diseases.

Through her intellectual leadership and groundbreaking science, Sara Wickström has propelled mechanobiology into a central position in contemporary biomedicine and laid a foundation for future clinical advances.

- Edvard Moser, Chair of the Körber Prize Search Committee Life Sciences