By Ren-Ke Li, Richard D. Weisel
Cardiac Regeneration and service, quantity One reports the pathology of cardiac damage and the most recent advances in mobile therapy.
Chapters partly one discover the pathogenesis of congestive middle failure, the mechanisms answerable for adversarial cardiac matrix home improvement, and strength interventions to revive ventricular functionality. half highlights new ways to mobile treatment for cardiac regeneration, and comprises chapters overlaying other ways of mobile supply, tracking phone engraftment, and the feasibility of utilizing allogeneic stem cells to revive cardiac functionality. Chapters partly 3 movement directly to spotlight novel stem cells for cardiac fix, together with human embryonic stem cells and human pluripotent stem cells, and aspect their present prestige and destiny capability for cardiac treatment. eventually, half 4 explores gene remedy, and contains ultrasound-targeted or direct gene supply in addition to cell-based gene treatment for cardiac regeneration.
Cardiac Regeneration and service, quantity One is complemented through a moment quantity overlaying biomaterials and tissue engineering. jointly, the 2 volumes of Cardiac Regeneration and Repair offer a entire source for clinicians, scientists, or academicians fascinated about cardiac regeneration, together with these drawn to telephone treatment, tissue engineering, or biomaterials.
- Explores the pathogenesis of congestive center failure, the mechanisms chargeable for opposed cardiac matrix home improvement, and strength interventions to revive ventricular function
- Highlights new methods to cellphone remedy for cardiac regeneration and comprises chapters protecting alternative ways of mobilephone supply, tracking cellphone engraftment, and the feasibility of utilizing allogeneic stem cells to revive cardiac function
- Explores gene remedy and comprises ultrasound-targeted or direct gene supply in addition to cell-based gene remedy for cardiac regeneration
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Extra info for Cardiac regeneration and repair: Pathology and therapies
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Galectin-3 (Gal-3), a 29–35-kDa soluble β-galactoside-binding lectin that plays a role in the regulation of cardiac fibrosis and remodeling, is emerging as a potentially important marker of cardiac fibrosis. 129 Gal-3 expression is increased in the infarct region at 7 days post-MI in mice130 and in both experimental131 and clinical132 HF. 41,115 Fibroblasts are the predominant non-myocyte cells in the heart and regulate ECM homeostasis in normal and diseased hearts. 10–12 Fibroblasts activated by signals in injury undergo phenotypic transformation into myofibroblasts that express contractile proteins, including a-smooth muscle actin, vimentin and desmin.
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