Our Speakers
The symposium features a panel of world-leading experts, studying the mechanisms of tissue repair with the aim to develop new treatments for fibrotic diseases.
Keynote Session
Fundamental Processes of Organ Repair After Injury
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University of Bristol, UK
Dr. Paul Martin
Wound healing: from fly to fish to mouse to man to cancer
Professor Paul Martin's lab models wound healing in several genetically tractable model organisms from the fruit fly, Drosophila, through to zebrafish and mice, with the ultimate goal of uncovering fundamental mechanisms that will enable development of wound healing therapeutics for human patients. We know that inflammation causes fibrosis and is also aberrant in chronic wounds and so we use Drosophila and translucent zebrafish models to make movies of leukocyte migration into the wound and to dissect the genetics of inflammatory cell recruitment towards tissue damage and its consequences. In Drosophila and mice we have used various approaches to identify re-epithelialisation genes and those associated with wound inflammation, in the hope that these might lead us towards therapeutic targets for kick-starting chronic wounds, and blocking inflammation-driven fibrosis, respectively.
Recently we have become interested also in exploring the parallels between wound healing and cancer, in particular investigating how the wound inflammatory response (as for example, triggered by biopsy or cancer surgery), might impact on immune cell recruitment to nearby transformed cells and what might be the downstream consequences of this.
More information on the research in the Martin lab is available at: https://www.bristol.ac.uk/biochemistry/research/martin-group/
Opening Session
Single Cell Contributions to Organ Repair and Fibrosis - the Big Picture
University of Edinburgh, UK
Dr. Neil Henderson
Using single cell genomics and spatial profiling to decode human liver injury and repair
Neil Henderson undertook medical training in Edinburgh and London before completing a Wellcome Trust funded PhD at the MRC Centre for Inflammation Research, Edinburgh. He then trained in hepatology and was awarded a Wellcome Trust Intermediate Fellowship, during which time he spent a 3 year post-doctoral period based at the University of California, San Francisco, USA. Neil was then awarded a Wellcome Trust Senior Research Fellowship in Clinical Science to investigate mechanisms of organ fibrosis and regeneration, using cutting-edge approaches including the rapidly evolving field of single cell genomics.
More information on the research in the Henderson lab is available at: https://www.ed.ac.uk/inflammation-research/people/principal-investigators/professor-neil-henderson
Session 1
Mechanical Aspects of Organ Repair and Fibrosis
Mayo Clinics, USA
Dr. Daniel Tschumperlin
Mechano-therapies to treat lung fibrosis
Daniel Tschumperlin, Ph.D. is Professor of Physiology and Biomedical Engineering at Mayo Clinic in Rochester, Minnesota. Dr. Tschumperlin earned his B.S. in Mechanical Engineering at Rice University and his M.S. and Ph.D. in Bioengineering at University of Pennsylvania. Prior to joining the Mayo Clinic Dr. Tschumperlin was a postdoctoral fellow and then faculty member at the Harvard School of Public Health. Dr. Tschumperlin’s research focuses on the respiratory system and how the structure, function and mechanics of the lung are regulated in health and disease. His laboratory has explored mechanobiological feedback mechanisms central to the pathogenesis of fibrotic diseases, and his recent work is directed at discovering and translating novel mechanisms by which fibrotic remodeling in the lung can be reversed.
More information on the research in the Tschumperlin lab is available at:
https://www.mayo.edu/research/labs/tissue-repair-mechanobiology/overview
Cornell University, USA
Dr. Jan Lammerding
New insights into nuclear mechanobiology in physiology and disease
Jan Lammerding is a Professor in the Meinig School of Biomedical Engineering and the Weill Institute for Cell and Molecular Biology at Cornell University. He received his Diplom Ingenieur degree in Mechanical Engineering from the University of Technology (RWTH) in Aachen, Germany, and completed his Ph.D. in Biological Engineering at the Massachusetts Institute of Technology. Dr. Lammerding served as a faculty member at Harvard Medical School/Brigham and Women’s Hospital before moving to Cornell University in 2011. The research in the Lammerding Laboratory is focused on ‘nuclear mechanobiology’, investigating how the mechanical properties of the nucleus modulate cellular functions, and how physical forces acting on the nucleus affect its structure and processes. The multidisciplinary research approach combines the development of novel experimental assays with cell and molecular biology techniques and in vivo models. Dr. Lammerding has published over 100 peer-reviewed articles, including in Nature, Science, and PNAS. Dr. Lammerding is a Fellow of the American Society for Cell Biology, the Biomedical Engineering Society, and the American Institute for Medical and Biological Engineering. His research is supported by awards from the National Institutes of Health (NIH), the National Science Foundation, and the Volkswagen Foundation.
More information on the research in the Lammerding lab is available at: http://lammerding.wicmb.cornell.edu/.
Session 2
What a Wounderful World: Skin and Kidney Repair and Fibrosis
University of Pennsylvania, USA
Dr. Katalin Susztak
Molecular pathways that drive diabetic kidney disease
Katalin Susztak, MD, PhD is a Professor of Medicine and Genetics at the University of Pennsylvania, she is a physician scientist who aims to understand the genetics and molecular mechanism of kidney disease development, with the ultimate goal of finding new, more effective therapies.
She has made discoveries fundamental towards defining critical genes, cell types and mechanisms of chronic kidney disease. She was instrumental in defining genetic, epigenetic and transcriptional changes in diseased human kidneys. She identified multiple novel kidney disease genes and demonstrated role of Notch signaling and metabolic dysregulation in kidney disease development.
Her lab was the first to map the kidney epigenome and catalogue genotype-driven gene-expression variation (eQTL) in human kidneys. Integration of genome-wide association studies
(GWAS), eQTL and epigenome data has been essential to prioritize disease-causing genes and variants.
Dr. Susztak generated the first unbiased, comprehensive kidney cell-type atlas using single cell transcriptomics. She identified that specific renal endophenotypes are linked and likely caused by the dysfunction of specific cell types.
In follow-up animal model studies, she conclusively demonstrated that MANBA, DAB2, DACH1 and APOL1 are new kidney disease risk genes. Her work established the role of proximal tubule cells, endolysosomal trafficking, metabolic and developmental pathways in kidney disease development.
Dr. Susztak's discoveries span genetics, genomics, epigenetics, molecular biology, physiology and nephrology, and have enormous translational relevance and considerable therapeutic potential.
Professor Susztak is member of the American Society of Clinical Investigators, American Associations of Physicians and recipient of the Osler Award of the University of Pennsylvania, Young Investigator Award of the American Society of Nephrology and Richards Award of the International Society of Nephrology.
University of Cologne, Germany
Dr. Sabine Eming
Immune-mediated tissue repair
The skin is constantly exposed to environmental stress factors such as injury, microbes, UV light and toxic substances. Therefore, by nature the skin is explicitly well furnished to restore tissue integrity and homeostasis following tissue damage. Cellular and molecular mechanisms that control tissue repair are complex and involve cell-cell and cell-matrix interactions directed by a network of soluble mediators. Furthermore, wound healing mechanisms are not unique to the tissue repair response. In fact, postnatal wound healing in part recapitulates processes in developmental biology and organogenesis. Signals controlling cell growth, migration and differentiation during tissue repair have also emerged as central mediators in cancer biology and other inflammatory disease processes.
Professor Eming leads a programme of work in tissue damage and repair that encompasses the range from basic structure-function analysis, through in vivo models, to human disease. The group is aiming at a deeper understanding on how the skin senses tissue damage and how these events translate into a regenerative response or disease. Our findings might provide the possibility to manipulate the healing response in order to readjust postnatal repair into regeneration and to develop novel strategies for pharmacological interventions in pathological healing conditions associated with diabetes mellitus, inflammatory diseases or ageing. In addition, we are interested to study the interrelation between tissue repair, mechanisms of cancer development and inflammatory skin diseases.
Session 3
The Good and The Bad of Regeneration
University of California San Diego, USA
Dr. Tatiana Kisseleva
Regression of cholestatic fibrosis
Dr. Kisseleva is a Professor of Surgery at University California San Diego, and Director of the Stem Cell Fitness and Space Medicine Center at the Sanford Stem Cell Fitness Institute. The major interest of her research is the identification of new targets for anti-fibrotic therapy for MASH and Met-ALD. Her lab studies the origin of myofibroblasts in fibrotic liver and investigates the contribution of activated Hepatic Stellate Cells (HSCs) and Portal fibroblasts/mesenchymal cells (aPFs) to hepatotoxic and cholestatic liver fibrosis. She has characterized IL-17 signaling in the pathogenesis of ALD and NASH-induced HCC. She developed techniques to isolate and study activated aPFs (Iwaisako, PNAS, 2012), identified novel markers of aPFs/mesenchymal cells, and demonstrated that interaction between Mesothelin, Mucin 16, and Thy-1 in the activation of aPFs (Koyama, JCI, 2017, Nishio, J. Hepatol., 2019, Nishio, PNAS, 2021). She developed techniques to purify and culture primary HSCs from human livers, as well as to study their subsets and transcriptional regulation using ChIP-seq, scRNA-seq and scATAC-seq (Liu, Gastroenterology, 2020).
More information on the research in the Kisseleva lab is available at: https://profiles.ucsd.edu/tatiana.kisseleva
University of Pennsylvania, USA
Dr. Ellen Puré
Cancer and its associated fibroblasts
Ellen Puré, Ph.D. is Grace Lansing Lambert Professor of Biomedical Sciences and Professor of Systems Pharmacology and Translational Therapeutics at the University of Pennsylvania. Dr. Puré received her Baccalaureate degree from Washington University in St. Louis, and doctorate from the University of Texas-Southwestern Medical School. She trained as a Damon Runyon-Walter Winchell Postdoctoral Fellow and Leukemia Society Special Fellow and then joined the Faculty at Rockefeller University in 1982. In 1992 she joined the Faculties of the Wistar Institute and University of Pennsylvania where she served as Chair of the Department of Biomedical Sciences from 2013 until 2023 and is Director of the Penn Vet Cancer
Center. Dr. Puré is an Associate Director of the Cancer Research Institute, serves on the editorial boards of the Journal of Clinical Investigation and Matrix Biology and is a Founding Senior Editor of Cancer Immunology Research. In 2019, Dr. Puré was named a Fellow of the American Association for the Advancement of Science (AAAS). She is a scientific co-founder of Capstan Therapeutics.
Dr. Puré studies mechanisms of chronic inflammation and fibrosis and the
contributions of these processes to fibrotic diseases and cancer. Her laboratory has made seminal contributions to our understanding of stromal cells and matrix remodeling in tissue fibrosis and cancer, including the concepts of stromal cell heterogeneity, of a stromagenic switch, and of stroma-dependent niches. Her lab showed in preclinical models that disrupting stroma can reverse fibrosis and restore tissue function and in the context of solid tumors, inhibit tumor growth and overcome therapeutic resistance. Based on their results regarding the mechanisms involved and bioinformatic analyses of receptor-ligand interactions that demonstrate dominance of stromal cell interactions with
other tissue/tumor components, they posit that the therapeutic effects are at least in part due to “normalization” of pathologic tissue/tumor microenvironments. Current goals include translation of a stroma-targeted chimeric antigen receptor (CAR) therapy to the clinic while further delineating mechanisms to inform the development of future complementary and alternative stroma-targeted approaches.
More information on the Puré research lab is available at: https://www.vet.upenn.edu/research/centers-laboratories/research-laboratory/research-laboratory/pure-laboratory
Session 4
Hearts : All you Need to Heal
University of Cincinnati, USA
Dr. Jeff Molkentin
At the heart of repair
Jeffery D. Molkentin, PhD. Is a Professor in the Department of pediatrics, University of Cincinnati and Cincinnati Children's Hospital in the United States of America. He received a PhD from the Medical College of Wisconsin in 1994, after which he performed postdoctoral training with Dr. Eric Olson in Texas (USA) from 1994-1997, followed by his first faculty appointment in 1997 at the Cincinnati Children’s Hospital
Dr. Molkentin has published over 440 original articles over his career, with a Scopus H-index of 130 and Google Scholar h-index of 156. Dr Molkentin has published several high impact manuscripts in Cell, Science, Nature over his career. Dr. Molkentin was a full investigator of the Howard Hughes Medical Institute in the USA from 2008-2021.
Dr Molkentin has placed 35 of his past trainees into academics as laboratory principal investigators, and another 30+ as leading scientists in the pharmaceutical industry and biotechnology industry. Dr Molkentin has also graduated 13 PhD or MD/PhD students from his laboratory.
With respect to funding, Dr Molkentin currently holds 7 NIH grants as PI or Project Director, and his laboratory has had at least 5 NIH grants as PI for the past 20 years.
The research program focuses on cardiovascular and skeletal muscle disease through examination of basic signaling mechanisms. His larger projects include defining the molecular mechanisms that underlie cell death, with a special interest in mitochondrial-dependent mechanisms of non-apoptotic death. The laboratory is also interested in characterizing the intracellular signaling pathways that control cellular growth, differentiation, and replication in cardiac and skeletal muscle. His laboratory is actively engaged in identifying novel secreted protein factors (cytokines, growth factors, chemokines, etc) from the heart and skeletal muscle that might control disease responsiveness. His laboratory is also actively engaged in studying the cardiac and skeletal muscle fibroblast and how it functions during disease to alter the extracellular matrix, which impacts tissue remodeling. More recently his laboratory has been investigating the cellular mechanisms underlying cardiac repair, predominantly through effects of the immune response in the heart and how it alters healing and fibroblast activity.