title: Personalizing cardiac regenerative therapy: At the heart of Pim1 kinase.
abstract: During cardiac aging, DNA damage and environmental stressors contribute to telomeric shortening and human cardiac progenitor cells acquire a senescent phenotype that leads to decreased stem cell function. Reversion of this phenotype through genetic modification is essential to advance regenerative therapy. Studies in the cardiac specific overexpression and subcellular targeting of Pim1 kinase demonstrate its influence on regeneration, proliferation, survival, metabolism and senescence. The cardioprotective effects of Pim1 modification can be picked apart and enhanced by targeting the kinase to distinct subcellular compartments, allowing for selection of specific phenotypic traits after molecular modification. In this perspective, we examine the therapeutic implications of Pim1 to encourage the personalization of cardiac regenerative therapy.
authors.affiliation: San Diego Heart Research Institute, San Diego State University, San Diego, CA 92182, United States.
authors.forename: Kaitlen
authors.initials: K
authors.lastname: Samse
authors.affiliation: San Diego Heart Research Institute, San Diego State University, San Diego, CA 92182, United States.
authors.forename: Nirmala
authors.initials: N
authors.lastname: Hariharan
authors.affiliation: San Diego Heart Research Institute, San Diego State University, San Diego, CA 92182, United States. Electronic address: heartman4ever@icloud.com.
authors.forename: Mark A
authors.initials: MA
authors.lastname: Sussman
mesh_terms: D000818:Animals; D006321:Heart / Q000502:physiology*; D006801:Humans; D009206:Myocardium / Q000378:metabolism*; D057285:Precision Medicine; D051573:Proto-Oncogene Proteins c-pim-1 / Q000378:metabolism*; D012038:Regeneration
chemical_list: C496634:PIM1 protein, human; D051573:Proto-Oncogene Proteins c-pim-1
keywords: Aging; Apoptosis; Heart failure; Human cardiac progenitor cell; Pim1; Senescence