Journal
EXPERT REVIEW OF CARDIOVASCULAR THERAPY
Volume 11, Issue 8, Pages 949-957Publisher
TAYLOR & FRANCIS INC
DOI: 10.1586/14779072.2013.814830
Keywords
cell therapy; cardiac progenitor cell gene therapy; heart failure; Pim-1; senescence
Categories
Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL117163, R21HL102613, R37HL091102, R21HL102714, R21HL104544, P01HL085577, R01HL113647, R01HL105759, R01HL067245, RC1HL100891] Funding Source: NIH RePORTER
- NHLBI NIH HHS [R01 HL113647, R21HL102613, RC1HL100891, R37HL091102, R37 HL091102, R01HL067245, P01HL085577, R01 HL117163, R21HL102714, R21 HL102714, R01HL105759, R21HL104544, R01 HL105759, RC1 HL100891, R21 HL102613, R21 HL104544, P01 HL085577, R01 HL067245] Funding Source: Medline
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Regenerative therapy in severe heart failure patients presents a challenging set of circumstances including a damaged myocardial environment that accelerates senescence in myocytes and cardiac progenitor cells. Failing myocardium suffers from deterioration of contractile function coupled with impaired regenerative potential that drives the heart toward decompensation. Efficacious regenerative cell therapy for severe heart failure requires disruption of this vicious circle that can be accomplished by alteration of the compromised myocyte phenotype and rejuvenation of progenitor cells. This review focuses upon potential for Pim-1 kinase to mitigate chronic heart failure by improving myocyte quality through preservation of mitochondrial integrity, prevention of hypertrophy and inhibition of apoptosis. In addition, cardiac progenitors engineered with Pim-1 possess enhanced regenerative potential, making Pim-1 an important player in future treatment of severe heart failure.
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