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Showing 1–3 of 3 results
Advanced filters: Author: "Richard T. Lee" Clear advanced filters
  • Myocardial infarction can cause irreversible heart muscle cell damage and lingering cardiac problems that can eventually lead to heart failure. For over a decade, researchers have been trying to coax stem cells to differentiate into cardiomyocytes to repair damaged heart tissue, with limited success. In 'Bedside to Bench', Christine L. Mummery and Richard T. Lee lay out a framework for re-evaluating cardiac cell therapies in the context of two recent clinical trials, in which autologous cardiac stem cells derived from heart biopsies were transferred into patients, with promising, albeit difficult to interpret, results. Results from previous clinical trials using autologous bone marrow–derived adult stem cells to induce cardiac regeneration add to the debate about how to cautiously move forward in the cardiac regeneration field and to the questions that need to be urgently answered at the bench. In 'Bench to Bedside', Young-Jae Nam, Kunhua Song and Eric N. Olson discuss a number of recent studies in rodents showing that cardiac fibroblasts can be reprogrammed, via miRNAs and a transcription factor 'cocktail', to express cardiac genes, which resulted in improved cardiac function in the animals, suggesting a new way forward for fixing damaged heart tissue.

    • Christine L Mummery
    • Richard T Lee
    Comments & Opinion
    Nature Medicine
    Volume: 19, P: 412-413
  • Ischaemic cardiomyopathy leads to destruction of cardiomyocytes beyond the regenerative potential of the adult human heart. The murine heart can regenerate in utero and shortly after birth, but oxidative stress eventually arrests cardiomyocyte division. Chronic hypoxia in mice has now been shown to induce the cell cycle in cardiomyocytes, resulting in cardiac regeneration.

    • Niranjana Natarajan
    • Richard T. Lee
    News & Views
    Nature Reviews Cardiology
    Volume: 14, P: 7-8
  • The recent discovery of the ST2 receptor ligand — interleukin-33 — has provided new insight into the importance of ST2 signalling as a mediator of inflammation. Now, an additional role for this pathway as a novel cardioprotective paracrine system is emerging. Here, Kakkar and Lee review these roles and discuss the therapeutic potential of targeting this pathway to treat associated diseases such as asthma, rheumatoid arthritis, atherosclerosis and heart failure.

    • Rahul Kakkar
    • Richard T. Lee
    Reviews
    Nature Reviews Drug Discovery
    Volume: 7, P: 827-840