For cardiovascular regeneration, more robust selection markers and refined experimental protocols are required to reproducibly guide iPSCs to a cardiovascular lineage.15, 18 Furthermore, effective negative selection against pluripotent cells is necessary to avoid teratoma formation by contaminating pluripotent stem cells.19 There is also the concern that autologous iPSC-derived cells may acquire genetic

or epigenetic alterations during the reprogramming or differentiation process and/or may recapitulate the vascular disease Inhibitors,research,lifescience,medical of the patient from which they were obtained. However, great strides have been made in refining iPSC generation since Shinya Yamanaka first used a retroviral approach to overexpress the reprogramming factors. 4, 6, 20 Because this approach Inhibitors,research,lifescience,medical raised concerns regarding the integration of foreign DNA in the host genome, effective nonviral strategies for induction of pluripotency were developed. Our group has employed protein-based approaches to deliver reprogramming factors for generating iPSCs. In doing so, we have discovered the effect of innate immune activation in effective reprogramming, a finding that will lead to therapeutic ramifications.20 Conclusion Induced pluripotent stem cells hold great promise

for cardiovascular regeneration because of their unlimited Inhibitors,research,lifescience,medical capacity for proliferation and differentiation. iPSC technology already has enabled an exciting new approach for disease modeling and drug screening. Despite the great progress, the clinical use of iPSC technology is still in its infancy, and many technical hurdles remain. Ultimately, we and others intend to develop personalized Inhibitors,research,lifescience,medical cell therapies in the treatment of peripheral artery and heart diseases.21, 22 Funding Statement Funding/Support: Dr. Cooke receives research funding from the National Institutes of Health, Dr. Sayed is supported Inhibitors,research,lifescience,medical by a NIH postdoctoral fellowship (HL098049-01A1)

and American Heart Association Scientist Development Grant (AHASDG) (13SDG17340025), and Dr. Wong is supported by a postdoctoral fellowship (12POST8830020) and Scientist Development Grant (13SDG15800004) from the American Heart Association. Footnotes Conflict of Interest Disclosure: The authors have completed and submitted the NVP-BGJ398 purchase Methodist DeBakey Cardiovascular Journal Conflict Ergoloid of Interest Statement and none were reported. Contributor Information Wing Tak Wong, Houston Methodist Hospital Research Institute, Houston Methodist Hospital, Houston, Texas. Nazish Sayed, Houston Methodist Hospital Research Institute, Houston Methodist Hospital, Houston, Texas. John P. Cooke, Houston Methodist Hospital Research Institute, Houston Methodist Hospital, Houston, Texas.
Introduction Cardiovascular disease is a major public health problem that imposes a huge economic burden on health systems around the world, and patients with end-stage heart failure (HF) represent a large share of the healthcare spending.