title: Cardioprotection by Targeting the Pool of Resident and Extracardiac Progenitors.
abstract: The adult heart has the capacity to generate new myocytes that are markedly enhanced in acute and chronic heart failure of ischemic and non-ischemic origin. In addition, a pool of blood trafficking progenitor cells able to sense myocardial damage may home to the sites of injury participating to cardiac repair. This new view of myocardial biology leads to an expanding long-term research and therapeutic goals for cardioprotection. A fundamental concept to be analyzed is whether cardiac diseases are influenced by changes in the properties of tissue specific and circulating progenitors. Loss of self-renewal capacity, impaired growth or increased susceptibility to death may lead to a reduction of progenitors and leave myocardial damage unrepaired. Cardiac progenitors generate all myocardial cell lineages, thus impairment in their growth is expected to be critically involved in the structural and functional modifications of the heart. The fact that, in addition to well known effects of anthracyclines, also new drugs that target molecular pathways implicated in cell death and growth can be cardiotoxic further supports our hypothesis. Understanding the role of resident and extracardiac progenitors in the pathogenesis of cardiomyopathies of different etiology will provide not only a better comprehension of cardiac homeostasis but will also open new avenues for therapeutic interventions. The progress toward effective myocardial regeneration based on exploiting the self-renewal potential of the myocardium and the systemic pool of cardiogenic cells should advance the likelihood of efficient cardioprotection and restoration of cardiac function.
authors.forename: Konrad
authors.initials: K
authors.lastname: Urbanek
authors.forename: Caterina
authors.initials: C
authors.lastname: Frati
authors.forename: Gallia
authors.initials: G
authors.lastname: Graiani
authors.forename: Denise
authors.initials: D
authors.lastname: Madeddu
authors.forename: Angela
authors.initials: A
authors.lastname: Falco
authors.forename: Stefano
authors.initials: S
authors.lastname: Cavalli
authors.forename: Bruno
authors.initials: B
authors.lastname: Lorusso
authors.forename: Andrea
authors.initials: A
authors.lastname: Gervasi
authors.forename: Lucia
authors.initials: L
authors.lastname: Prezioso
authors.forename: Monia
authors.initials: M
authors.lastname: Savi
authors.forename: Francesca
authors.initials: F
authors.lastname: Ferraro
authors.forename: Federica
authors.initials: F
authors.lastname: Galaverna
authors.forename: Pietro
authors.initials: P
authors.lastname: Rossetti
authors.forename: Costanza Annamaria
authors.initials: CA
authors.lastname: Lagrasta
authors.forename: Fancesca
authors.initials: F
authors.lastname: Re
authors.forename: Eugenio
authors.initials: E
authors.lastname: Quaini
authors.forename: Francesco
authors.initials: F
authors.lastname: Rossi
authors.forename: Antonella De
authors.initials: AD
authors.lastname: Angelis
authors.affiliation: Department of Clinical and Experimental Medicine, University-Hospital of Parma, Via Gramsci, 14, 43126 Parma, Italy. federico.quaini@unipr.it.
authors.forename: Federico
authors.initials: F
authors.lastname: Quaini
mesh_terms: D002316:Cardiotonic Agents / Q000494:pharmacology*; D016923:Cell Death / Q000187:drug effects; D006331:Heart Diseases / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D006801:Humans; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000502:physiology; D044968:Regenerative Medicine; D033581:Stem Cell Transplantation; D013234:Stem Cells / Q000187:drug effects / Q000502:physiology*
chemical_list: D002316:Cardiotonic Agents