Prof. Elisabeth Engel López leads the Biomaterials for Regenerative Therapies group at the Institute for Bioengineering of Catalonia (IBEC) and serves as a Professor at the Technical University of Catalonia. With over 80 publications in JCR journals, her work focuses on designing biomaterials and scaffolds for in vitro/in vivo regenerative medicine, emphasizing cellular response mechanisms and translational applications. Developing lactate-releasing systems for metabolic modulation Advancing 3D bioprinting for tissue-specific models Engineering angiogenic and osteogenic biomaterials Her research bridges fundamental studies with industrial partnerships, including pharmaceutical and biomedical device companies, and contributes to European collaborative projects. She received the Barcelona City Award for technological research and has delivered numerous invited lectures. Her group explores substrate stiffness, ion release, and microenvironmental cues to control cell behavior in cardiac, neural, and bone regeneration contexts.
Xiaochen He serves as an Instructor in the Department of Physiology & Biophysics at the University of Mississippi Medical Center's School of Medicine, where he focuses on cardiovascular research and teaching within this foundational medical science department. His research program centers on the intersection of cardiac pathophysiology and immunometabolism, with core interests including: Mechanisms of immune-mediated cardiac inflammation in heart failure Role of T cell subsets (Th17, γδ T, CD8+) in pressure overload models Molecular regulation by IL-12 family cytokines and metabolic enzymes (TIGAR, SIRT3) Endothelial dysfunction in cardiac hypertrophy and failure progression Therapeutic interventions targeting inflammatory pathways Analysis of Dr. He's recent publications (2022-2025) reveals a concentrated research trajectory investigating how specific immune pathways drive heart failure progression. His work consistently employs genetic mouse models to demonstrate that IL-12β inhibition, TIGAR deficiency, and selenium supplementation attenuate cardiac inflammation and dysfunction, while CD8+ T cell metabolic reprogramming exacerbates disease. Key discoveries include GPR174's role in Th17 differentiation and NK1.1 signaling's contribution to cardiopulmonary inflammation, establishing critical immune-metabolic axes in heart failure pathogenesis. No scientific awards were documented in the available profile information. Current departmental records indicate no graduate students are formally listed under Dr. He's mentorship, and no research grants are specified in the public profile. Details regarding laboratory infrastructure, research teams, or collaborative networks were not provided in the available institutional documentation.
Dr. Jingsong Zhou is a Professor of Kinesiology and Associate Director of the Bone-Muscle Research Center at The University of Texas at Arlington. Her research focuses on neuromuscular diseases, particularly Amyotrophic Lateral Sclerosis (ALS), with expertise in striated muscle physiology, calcium signaling, and mitochondrial dysfunction. She leads the Neuromuscular Diseases Lab, which develops genetic mouse models and molecular probes to study ALS mechanisms. Dr. Zhou’s work has been supported by NIH, MDA, DOD, and the ALS Association. She serves on the NIH SMEP study section and has over 20 years of academic experience, including postdoctoral training at Vanderbilt University College of Medicine and a PhD from Rush University School of Medicine. Education: Postdoctoral Fellow in Pharmacology, Vanderbilt University College of Medicine (2001) PhD in Molecular Biophysics and Physiology, Rush University School of Medicine (1997) Diploma in Medicine, Hunan Medical University (Xiangya Medical School) (1986) Research Interests: Mechanisms of calcium signaling and mitochondrial dysfunction in ALS Role of sarcolemma repair and autophagy in neuromuscular disease progression Development of therapeutic strategies targeting mitochondrial health and membrane integrity Grants and Funding: NIH grants focused on ALS pathogenesis and muscle-bone interactions Support from MDA, DOD, and ALS Association for translational research projects Labs and Teams: Director of the Neuromuscular Diseases Lab at UT Arlington Collaborations in developing mouse models and molecular tools for ALS research
Paul W Burridge, PhD is an Associate Professor in the Department of Pharmacology at Northwestern University's Feinberg School of Medicine and a founding faculty member of the Center for Pharmacogenomics. His laboratory specializes in human induced pluripotent stem cell (hiPSC) modeling for pharmacogenomics and cardio-oncology research. Dr. Burridge's research focuses on understanding how genomic variation influences drug efficacy and toxicity, particularly in cancer therapy-induced cardiovascular complications. His lab pioneered several key methodologies including the first directed cardiac differentiation protocol, non-integrating blood-to-iPSC reprogramming, and chemically defined differentiation protocols. Current projects span cardio-oncology, arrhythmia mechanisms, regenerative medicine, hiPSC models of breast cancer, and cultivated meat applications. Analysis of his 15 most recent publications reveals a strong emphasis on pharmacogenomics of anthracycline cardiotoxicity, with significant focus on genomic risk prediction in childhood cancer survivors, molecular mechanisms of cardiotoxicity, and development of cardioprotective strategies. His work increasingly integrates large-scale genomic analysis with hiPSC modeling to establish causal relationships between genetic variants and clinical outcomes. Fellow of American Heart Association (2016) Recipient of NCI R01 grant for Nilotinib Induced Artery Disease research NIH NHLBI Pathway to Independence Award recipient Editorial Board Member, Journal of Molecular and Cellular Cardiology (2020-present) Associate Editor, JACC CardioOncology (2018-present) Dr. Burridge advises multiple postdoctoral fellows including Ning Ge (cardiac arrhythmia modeling), Praeploy Pongpamorn (chemically defined differentiation), Nnamdi Uche (population-specific doxorubicin susceptibility), and George Gibbons. His lab has secured substantial grant funding for projects including large-scale hiPSC production, cardiotoxicity screening platforms, and novel drug discovery initiatives. The Burridge lab maintains extensive resources including high-throughput screening systems, CRISPR editing platforms, and bioreactor-based differentiation systems, all developed with a focus on eliminating animal-derived products from research.
Professor Stuart Rushworth is a faculty member at Norwich Medical School, University of East Anglia, where he serves as the scientific group leader for molecular haematology research. His work focuses on the tumour microenvironment in haematological malignancies, particularly Acute Myeloid Leukaemia and Multiple Myeloma, and the impact of infection and ageing on haematopoietic stem cells. Education: Bachelor's Degree – University of Sunderland PhD in Immunology – University of Cambridge Post-doctoral Training – University of Cambridge and University of East Anglia His research explores metabolic reprogramming, mitochondrial transfer, and stromal interactions in cancer. He has made significant contributions to understanding how leukaemia cells exploit the bone marrow microenvironment for survival and proliferation. His studies have identified key mechanisms such as fatty acid release from adipocytes and intercellular mitochondrial transfer via tunnelling nanotubes. His work bridges basic science and clinical translation, with implications for drug resistance and novel therapeutic strategies. The most recent articles highlight trends in immunometabolism, infection-induced haematopoietic stress responses, and metabolic crosstalk in cancer. Key themes include mitochondrial dynamics, metabolic adaptation, and innate immune signaling pathways like STING. His publications appear in high-impact journals such as Cell Reports , Nature Communications , and Blood . He is actively funded by major research bodies including the British Heart Foundation, The Big C Appeal, Academy of Medical Sciences, and BBSRC. While no formal scientific awards are listed in the provided text, his research has led to clinical trials involving BTK inhibitors in myeloma patients. Professor Rushworth mentors several PhD researchers, including Dominic Fowler-Shorten, E. E. Wojtowicz, A. Jibril, J. A. Moore, and J. Mistry. He leads the Rushworth Group, which is part of the Metabolic Health Research Centre at UEA, focusing on metabolic processes in the tumour microenvironment.
Pilar Alcaide is a Professor of Immunology at Tufts University School of Medicine. Her research focuses on understanding molecular mechanisms of T lymphocyte trafficking in inflammatory heart diseases, particularly heart failure. She combines immunology, vascular biology, and cardiac physiology to investigate immune-cardiac interactions using mouse models and advanced microscopy techniques. Education: Ph.D. and M.S. in Immunology from Universidad Autónoma de Madrid (Spain) Dr. Alcaide's lab explores how T cell-endothelial interactions contribute to cardiac pathophysiology, with translational goals toward developing immune-based therapeutics. Key areas include: STING signaling in microglial-neuronal interactions Myeloid fatty acid metabolism in HFpEF CXCR3 blockade for immunotherapy myocarditis Her work has been funded by NIH grants (e.g., mechanisms of T cell activation in cardiac fibrosis). Notable awards include the ASIP Cotran Early Career Investigator Award.
Quansheng Du is an Associate Professor at the Medical College of Georgia , affiliated with the Department of Neuroscience and Regenerative Medicine and the Department of Neurology . His academic appointments include teaching responsibilities in advanced molecular biology courses such as BIOM 8230 Biology of Proteins in Disease and BIOM 8022 Molecular Cell Biology . Education: Ph.D., Molecular Biology, Wuhan University (1999) MS, Molecular Biology, Wuhan University (1995) Research Interests span molecular mechanisms in neurological diseases, regenerative medicine, and metabolic pathways in cancer cachexia. His work includes studies on genetic disorders (MRKH syndrome), microRNA roles in neuronal survival, purine synthesis inhibition in pulmonary hypertension, and TEAD1 signaling in cardiomyocyte protection. Recent Publications (2021–2024) focus on molecular biology intersections with neuroscience, cardiovascular diseases, and cancer metabolism, with recurring themes in genetic regulation, cellular reprogramming, and metabolic dysregulation.
Mark Crabtree is a University Research Lecturer and British Heart Foundation Intermediate Basic Science Research Fellow at the University of Oxford, leading the Channon Group focused on cardiovascular functional genomics and redox signaling. His research integrates metabolomic and proteomic approaches to study nitric oxide mechanisms in cardiovascular disease models. Education: BSc (Hons) from the University of Surrey (2001), followed by a collaborative PhD at the University of Surrey and Weill Medical College of Cornell University. Postdoctoral training under Professor Keith Channon began in 2006, supported by a BHF Centre of Research Excellence Transition Fellowship (2012–2015). Research interests include nitric oxide delivery systems for cardiovascular therapies, redox signaling in cardiac injury, and tetrahydrobiopterin's role in metabolic regulation. His work bridges nanomaterials development (e.g., graphene-based NO-releasing coatings) with clinical applications in ischemia-reperfusion injury and atherosclerosis. Notable contributions include advancements in pH-sensitive NO delivery systems and mechanistic insights into myocardial nitroso-redox imbalance post-cardiac surgery. He chairs the 2018 International Nitric Oxide Society Conference and serves on the society's council. Scientific awards: British Heart Foundation Intermediate Basic Science Research Fellowship. Active grants include BHF funding for redox signaling studies. His lab collaborates internationally, with recent publications spanning NO-based therapies, metabolic reprogramming in macrophages, and vascular biology.
Jörg Menche holds a full Professor position (Univ.-Prof.) at the University of Vienna, with dual appointments in the Faculty of Mathematics, Department of Mathematics, and Max Perutz Labs, Department of Structural and Computational Biology. His work bridges mathematical modeling and biomedical research through network-based approaches to complex disease mechanisms. Primary research interests include Network Biology, Computational Systems Medicine, and Immunometabolism, with specific focus on proteomic signatures in neuropathic pain, metabolic reprogramming in obesity, and autoimmunity networks. He develops innovative computational tools like VRNetzer for virtual reality network analysis and BioProfiling.jl for high-content imaging data integration, targeting intersections between metabolism, immunity, and environmental exposures. Recent publications (2019-2024) reveal a dominant trend in multi-omics network medicine, particularly in autoimmunity (AutoCore framework), cardiometabolic diseases, and rare genetic disorders. His work demonstrates exceptional translational impact, with multiple papers highlighted by news outlets and patents (e.g., 3 patents referencing 2021 research). While the text indicates involvement in one project (2016) and 13 activities, grant specifics and student mentoring details remain undisclosed. His collaborative network spans immunology, neuroscience, and toxicology, evidenced by co-authorships with clinical and computational teams. Menche operates within Max Perutz Labs, a premier molecular biology research center in Vienna. His team integrates computational biologists, cell biologists, and clinicians to develop network cartography methods for disease module identification, with strong emphasis on virtual reality interfaces and multi-omics validation.
Dr. Narasimman Gurusamy is an Assistant Professor at the Barry and Judy Silverman College of Pharmacy, Nova Southeastern University, specializing in Pharmaceutical Sciences. He holds a Ph.D. in Pharmaceutical Sciences from Niigata University of Pharmacy and Applied Life Sciences (Japan) and completed postdoctoral training at UConn Health Center, Harvard Medical School, and University of Tennessee Health Science Center. Education: M.Pharm (Tamil Nadu Dr. MGR Medical University, India), Ph.D. (Niigata University, Japan) Research Focus: Epigenetic mechanisms in cardiac diseases, non-coding RNA regulation, exosome therapy, stem cell biology, and gene-environment interactions His work explores how long non-coding RNAs and epigenetic modifiers influence cardiac repair, particularly through induced mesenchymal stem cells and their exosomal signaling . Current projects investigate dietary and environmental impacts on epigenetic changes in the heart. Recent publications highlight advancements in RNA-based therapies and metabolic interventions for cardioprotection. Scientific Awards: American Heart Association Career Development Award, Young Research Scientist Award, Travel Awards Dr. Gurusamy serves as Grant Reviewer for the American Heart Association, Associate Editor for Frontiers in Cardiovascular Medicine , and Vice-Chair for the Communication Committee of the Society for South Asian Heart Research (SAHR). His lab employs in-vitro, in-vivo, and clinical trial approaches, utilizing PCR, ELISA, flow cytometry, and genomic repository analyses.
James C. Lo, M.D., Ph.D., is the Rohr Family Clinical Scholar and Associate Professor of Medicine at Weill Cornell Medical College . As a physician-scientist, he directs a basic research laboratory investigating the molecular basis of cardiometabolic diseases. 2023 : Rohr Family Clinical Scholar 2023 : Associate Professor of Medicine, Weill Cornell Medical College 2021 : Assistant Professor of Medicine, Weill Cornell Medical College Education: 2006 - M.D., University of Chicago Pritzker School of Medicine 2004 - Ph.D., University of Chicago 1998 - B.S., University of Chicago Dr. Lo's research focuses on molecular mechanisms of metabolic diseases with emphasis on: Cardiovascular biology in diabetes and obesity Adipose tissue function and thermogenesis Pancreatic islet physiology in metabolic stress Inter-organ communication networks Novel therapeutic targets for diabetes Cardiac complications in metabolic disorders Complement system in endocrine regulation His lab employs single-cell RNA-seq , genetic models , and multi-omics approaches to study: β cell subpopulations in diabetes Complement receptor signaling Adipose-liver-heart cross-talk Extracellular vesicle-mediated dysfunction Sex-dependent metabolic regulation Scientific Contributions: First to identify adipsin's role in β cell protection Discovered complement system's role in islet function Defined adipose tissue as SARS-CoV-2 target Elucidated mechanisms of obesity-induced arrhythmias Developed cross-species models of metabolic stress Research Funding: Currently holds 8 major grants as Principal Investigator or Key Personnel, including: $2.1M - NIH/NHLBI Mechanisms of Obesity-induced Atrial Fibrillation (2025-2028) $2.8M - NIH/NIDDK NAD+ Metabolism in β Cell Dysfunction (2025-2030) $1.5M - AHA Obesity-Driven Atrial Fibrillation (2024-2027) $1.2M - AHA Zebrafish Heart Regeneration (2023-2026) His laboratory team at the Belfer Research Building (New York, NY) includes post-doctoral fellows, Ph.D. students, medical students, and research technicians working in a collaborative environment.
Lisa Heather is an Associate Professor and British Heart Foundation (BHF) Intermediate Fellow at the University of Oxford's Department of Physiology, Anatomy, and Genetics (DPAG) within the Medical Sciences Division. Her research focuses on cardiac metabolism in health and disease, particularly in diabetes and heart failure. She holds dual expertise in molecular mechanisms of metabolic dysfunction and translational cardiovascular research. Dr. Heather earned a Bachelor's degree in Medical Biochemistry from the University of Surrey and conducted doctoral research on cardiac hypertrophy's metabolic origins. Her postdoctoral work explored mitochondrial dysfunction in diabetic cardiomyopathy. Key career milestones include a Diabetes UK RD Lawrence Fellowship (2011) and a BHF Intermediate Fellowship (2018), supporting her investigations into lipid metabolism and hypoxia signaling in diabetic hearts. Her research interests span mitochondrial bioenergetics, fatty acid trafficking, hypoxia responses, and metabolic reprogramming in disease. She employs advanced techniques like hyperpolarized MRI and metabolomics to study real-time metabolic changes, with recent breakthroughs identifying novel roles for fatty acids in disrupting hypoxia signaling and cardiomyocyte function. Her publications (e.g., Diabetes , Physiological Reviews , JCI Insight ) highlight interdisciplinary approaches to metabolic disease. She leads the Heather Group, advancing therapies targeting metabolic pathways in heart failure and diabetes. Her work bridges basic science and clinical applications, emphasizing metabolic interventions for cardiovascular health.
Jr. Prof. Dr. Elena S. Reckzeh leads the Department of Organoid and Chemical Biology at the University of Bonn's Life & Medical Sciences Institute (LIMES). Her research focuses on organoid-based models to study cancer metabolism and nutrient absorption mechanisms, with a particular emphasis on colorectal cancer. She integrates chemical biology approaches to identify small-molecule inhibitors targeting metabolic pathways linked to chemoresistance. Her work combines patient-derived tumor organoids with advanced screening techniques to develop compounds that disrupt metabolic flexibility in cancer cells. She also explores intestinal nutrient bioavailability using co-culture systems and synthetic biology tools. Key collaborations involve ESQlabs and the BMBF-funded project on personalized colorectal cancer therapy. Argelander Professorship (2023) BMBF Grant for personalized cancer therapy development Her lab’s innovations include micro-organosphere tissue engineering and pseudo-natural product inhibitors of glucose transporters. Current projects address metabolic plasticity in tumors, microbiome interactions in nutrient absorption, and translational applications in metabolic disease prevention.
Caius Gabriel Radu is a Professor in the Department of Molecular and Medical Pharmacology and the Department of Surgery at the University of California Los Angeles (UCLA) School of Medicine. His research program focuses on understanding fundamental biological processes at the interface between metabolic and signal transduction networks in cancer, immune cells, and stromal cells, with the goal of developing new diagnostic and therapeutic approaches. Dr. Radu's research expertise spans cancer immunobiology, immunotherapy, nucleotide metabolism, and molecular imaging. His laboratory has established a highly integrated research program that includes state-of-the-art instrumentation for Positron Emission Tomography (PET) and Mass Spectrometry platforms for metabolomics, proteomics, and phosphoproteomics. His interdisciplinary team collaborates with experts across UCLA and other institutions in molecular imaging, cancer metabolism, immunobiology, signal transduction, structural biology, radiochemistry, medicinal chemistry, and virology. Dr. Radu's research has led to significant discoveries, including uncovering a new role for the nucleoside salvage pathway in hematopoiesis, developing new PET probes for nucleotide metabolism (some of which have been translated to clinical use), and discovering novel small molecule inhibitors of metabolic kinases. One of these inhibitors has entered Phase I clinical trials (NCT05055609) for selected solid tumors and autoimmune disorders. His work also focuses on the immunobiology of pancreatic and prostate cancers, seeking to identify novel immunometabolic checkpoints that could be pharmacologically modulated alone or in combination with other therapies. Challenge Award, Prostate Cancer Foundation, 2017-2019 Challenge Award, Prostate Cancer Foundation, 2019-2021 Dr. Radu is currently Principal Investigator or Multiple Principal Investigator on multiple NIH-funded research projects, including studies on innovative mRNA vaccines for solid tumors, adenosine signaling in pancreatic cancer, PSMA-targeted radiopharmaceutical therapy, and targeting KRAS and adenosine-mediated immunosuppression. In collaboration with Dr. Norbert Pardi at UPenn, he has established a platform for evaluating mRNA lipid nanoparticle platforms for cancer immunotherapy.
Bradley McConnell is a Professor of Pharmacology and Assistant Chair in the Department of Pharmacological and Pharmaceutical Sciences at the University of Houston College of Pharmacy. He holds joint faculty appointments in the Department of Biology and Biochemistry (College of Natural Sciences and Mathematics) and is affiliated with multiple institutes including the Drug Discovery Institute (UH), Cardiovascular Research Institute (Baylor College of Medicine), and the Gulf Coast Consortia (Texas Medical Center). Education: B.S. in Biology (Pennsylvania State University), Ph.D. in Physiology and Biophysics (Case Western Reserve University), and Postdoctoral Fellow in Genetics (Harvard Medical School/Howard Hughes Medical Institute). Research focuses on cardiac signaling mechanisms in normal and diseased hearts, including β-adrenergic receptor signaling, AKAP-mediated pathways, and cell-based therapies for cardiac repair. Key projects involve reprogramming progenitor cells into functional cardiac cells, biased signaling studies, and understanding AKAP 'signalosomes' in cAMP pathways. His awards include the American Physiological Society Fellow (2014), American Heart Association Fellow (2011), and multiple teaching/mentoring awards from UH. He chairs the ASPET Cardiovascular Pharmacology Programming Committee and participates in national peer review committees. McConnell collaborates across disciplines through memberships in the Cougar Chairs Leadership Academy and National Center for Faculty Development. His lab integrates translational approaches—combining molecular biology, mouse models, and clinical insights—to advance heart repair therapies.
