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      Striated muscle function, regeneration, and repair

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      Cellular and Molecular Life Sciences
      Springer Nature

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          Abstract

          <p class="first" id="P2">As the only striated muscle tissues in the body, skeletal and cardiac muscle share numerous structural and functional characteristics, while exhibiting vastly different size and regenerative potential. Healthy skeletal muscle harbors a robust regenerative response that becomes inadequate after large muscle loss or in degenerative pathologies and aging. In contrast, the mammalian heart loses its regenerative capacity shortly after birth, leaving it susceptible to permanent damage by acute injury or chronic disease. In this review, we compare and contrast the physiology and regenerative potential of native skeletal and cardiac muscles, mechanisms underlying striated muscle dysfunction, and bioengineering strategies to treat muscle disorders. We focus on different sources for cellular therapy, biomaterials to augment the endogenous regenerative response, and progress in engineering and application of mature striated muscle tissues <i>in vitro</i> and <i>in vivo</i>. Finally, we discuss the challenges and perspectives in translating muscle bioengineering strategies to clinical practice. </p>

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          Left Ventricular Remodeling After Myocardial Infarction: Pathophysiology and Therapy

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            Macrophages are required for neonatal heart regeneration.

            Myocardial infarction (MI) leads to cardiomyocyte death, which triggers an immune response that clears debris and restores tissue integrity. In the adult heart, the immune system facilitates scar formation, which repairs the damaged myocardium but compromises cardiac function. In neonatal mice, the heart can regenerate fully without scarring following MI; however, this regenerative capacity is lost by P7. The signals that govern neonatal heart regeneration are unknown. By comparing the immune response to MI in mice at P1 and P14, we identified differences in the magnitude and kinetics of monocyte and macrophage responses to injury. Using a cell-depletion model, we determined that heart regeneration and neoangiogenesis following MI depends on neonatal macrophages. Neonates depleted of macrophages were unable to regenerate myocardia and formed fibrotic scars, resulting in reduced cardiac function and angiogenesis. Immunophenotyping and gene expression profiling of cardiac macrophages from regenerating and nonregenerating hearts indicated that regenerative macrophages have a unique polarization phenotype and secrete numerous soluble factors that may facilitate the formation of new myocardium. Our findings suggest that macrophages provide necessary signals to drive angiogenesis and regeneration of the neonatal mouse heart. Modulating inflammation may provide a key therapeutic strategy to support heart regeneration.
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              Heart failure.

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                Author and article information

                Journal
                Cellular and Molecular Life Sciences
                Cell. Mol. Life Sci.
                Springer Nature
                1420-682X
                1420-9071
                November 2016
                June 6 2016
                November 2016
                : 73
                : 22
                : 4175-4202
                Article
                10.1007/s00018-016-2285-z
                5056123
                27271751
                1f198990-ee7c-498b-9fa9-4420e7720913
                © 2016

                http://www.springer.com/tdm

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