Cellular and Molecular Bioengineering Conference ( Free PDF )

Content

  • BMES CMBE UNCLASSIFIED GROUP
  • BMES MANAGEMENT
  • SPECIAL COUNCIL BMES CMBE
  • NEXT MEETING CO-CHAIR
  • IMPORTANT INFORMATION
  • PROGRAM ACCESS
  • PLAN
  • KEY SPEAKERS
  • RECORDED SOURCES
  • SPONSOR INFORMATION
  • NOTE

Preface

Over the past century, remarkable advances in medicine and public health have contributed to dramatic improvements in the quality of life. Diseases of aging are now the leading cause of death in humans1. However, there are limitations to disease-specific treatment because the disease develops in parallel with many chronic diseases and because treatment of a single disease often contributes significantly to the total disease burden. As a result, diseases of aging are more common and more difficult to treat in older patients. We are now faced with a challenge where adult medicine is increasingly changing.

Anti-aging therapies offer great potential in combating aging-related diseases. However, in order to control, slow down or reverse aging, it is necessary to understand the basic mechanisms of aging. For example, it is now widely accepted that epigenetic information is gradually lost throughout the life cycle of organisms2, disrupting cellular homeostasis. Epigenetic biomarkers of aging (old clocks) can estimate the age of organisms with a variety of training methods, even if based solely on changes in DNA methylation during aging3. Interestingly, regaining of epigenetic information lost during natural reproduction and cell cycle replication4,5,6 that occurs during early pregnancy can be seen. This strategy is consistent with the concept of reprogramming-induced renewal (RIR)7, a recently discovered study in which older cells can revert to a more youthful state through prescription or medical treatment8,9. RIR is usually achieved through partial replication, a process by which stem cells differentiate into proliferating progenitor cells (iPSCs) 10, 11, 12, 13, 14, 15, 16. In this Perspective, we discuss recent advances in this field, provide insight into how it relates to the nature of aging and resilience, and highlight the advantages and disadvantages and explanatory potential of this RIR.

Partial cell reprogramming has been shown to increase the function of human muscle cells10, alter the aging mouse metabolome in vivo11, restore human dermal fibroblasts to higher levels -12 and alter the epigenetic clock in vitro10,12,13. Restore functional capacity of mice, prevent age-related changes in genetics, and extend the lifespan of wild-type mice. The clinical potential of partial resections undeniable, but the technology has its pitfalls. We discuss the future direction of therapeutic software and the biological mechanisms supporting RIR. Finally, we discuss the safety issues of partial resection and the importance of RIR separation.

Possible treatment for partial recurrence Partial regeneration has therapeutic potential due to its ability to renew cells. There are two basic methods that can help determine how to treat this condition. Biological regeneration is a complex but also direct method due to its ability to counteract aging in a way that does not depend on the properties of the cells used. Anti-aging techniques offer the potential to produce drugs that are more effective and efficient than those aimed solely at slowing aging. Biological regeneration can be achieved in two ways. First, direct modification of the microbiome could give each cell an adult body with 4 Fs (OSKM, Yamanaka’s four factors), but modifying the human genome is currently prohibited for safety and ethical reasons. Other methods include delivering Yamanaka elements in DNA or mRNA form with systems used in gene therapy. The functionality of the system is limited due to the limited capacity of existing distribution systems in some specific areas, which is inadequate17. However, with further progress in this approach, more efficient and effective stem cell treatments will become possible. To date, most in vivo cell-based studies have performed the full biological range in chimeric OSKM-deficient mice 8,11,15,18 except where the AAV9 delivery system was used for the delivery of the OSK16 factor. Since partial reprogramming is expected to produce different results in different areas, tissue- or system-specific reprogramming is more likely to lead to better results as a therapeutic measure in the near future.

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