Publications by authors named "Kaitlen Samse"

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.

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Human cardiac progenitor cells (hCPC) improve heart function after autologous transfer in heart failure patients. Regenerative potential of hCPCs is severely limited with age, requiring genetic modification to enhance therapeutic potential. A legacy of work from our laboratory with Pim1 kinase reveals effects on proliferation, survival, metabolism, and rejuvenation of hCPCs in vitro and in vivo.

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Article Synopsis
  • The study investigates how nucleostemin (NS) influences the regenerative capabilities of cardiac progenitor cells (CPCs) and its role in counteracting aging and senescence.
  • Findings reveal that older adult human CPCs show reduced NS expression, leading to senescence characteristics similar to those of older mouse CPCs, including decreased proliferation and increased cell flattening.
  • Overexpressing NS in older CPCs can restore their "stemness" properties and counteract aspects of aging, suggesting that targeting NS may enhance CPC-based therapies in elderly patients.
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Article Synopsis
  • The study investigates how the loss of Pim kinases contributes to cardiac aging by impairing mitochondrial function and energy production.
  • It finds that genetic deletion of Pim kinases in mice leads to early signs of heart failure, metabolic dysfunction, and cellular changes associated with aging.
  • The research concludes that Pim kinases play a crucial role in protecting heart health and maintaining mitochondrial integrity, offering insights that could help counteract cardiac aging.
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