Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Viewpoint
  • Published:

The next frontier in cardiovascular developmental biology—an integrated approach to adult disease?

Nature Clinical Practice Cardiovascular Medicine volume 4, pages 60–61 (2007)Cite this article

For centuries, clinicians and basic scientists worked side by side in a common quest to identify, understand, and heal the sicknesses of the day. Since the mid-twentieth century, however, a wedge has been slowly driven between these disciplines. Clinicians, constrained by demands incumbent on newly survivable conditions and an ever increasing knowledge base, have become inhibited from participating in basic scientific inquiry, while basic scientists have increasingly pursued more focused studies that result in less clinical translation. These trends are disturbing because of the fundamental need each profession has for the other. One clear example of the interdependent nature of these disciplines is developmental biology. Before the advent of powerful imaging techniques, such as ultrasound and MRI, clinicians were completely dependent on basic scientists to understand embryonic and fetal development.

Cardiac disease remains the number one cause of death from congenital malformations in infancy and accounts for 45–50% of post-neonatal deaths due to congenital anomalies in the US.1 Over the last 30 years, developmental biologists have worked to identify the morphogenic events and mechanisms of cardiovascular development. They have, however, placed much effort on the generation of mutant mice, with the hope of creating embryonically lethal phenotypes that highlight the importance of a particular gene, but which have little clinical utility. Developmental biologists are only now beginning to understand that it is a balance between signaling proteins, transcription factors, and a host of metabolic events, which determines the formation (and homeostasis) of structure. Most importantly, the complexity and balance of signals that affect processes controlling the formation of the heart also come into play in adult life, where their re-expression can be associated with the ability of heart cells to adapt to physiological or pathological stimuli.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

References

  1. Thom T et al. (2006) Heart disease and stroke statistics—2006 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 113: e85–e151

    PubMed  Google Scholar 

  2. Eisenberg LM and Markwald RR (1995) Molecular regulation of atrioventricular valvuloseptal morphogenesis. Circ Res 77: 1–6

    Article  CAS  Google Scholar 

  3. Rios H et al. (2005) periostin null mice exhibit dwarfism, incisor enamel defects, and an early-onset periodontal disease-like phenotype. Mol Cell Biol 25: 11131–11144

    Article  CAS  Google Scholar 

  4. Katsuragi N et al. (2004) Periostin as a novel factor responsible for ventricular dilation. Circulation 110: 1806–1813

    Article  CAS  Google Scholar 

  5. Xu Q et al. (2003) Circulating progenitor cells regenerate endothelium of vein graft atherosclerosis, which is diminished in ApoE-deficient mice. Circ Res 93: e76–e86

    Article  Google Scholar 

  6. Ikari Y et al. (1999) Neonatal intima formation in the human coronary artery. Arterioscler Thromb Vasc Biol 19: 2036–2040

    Article  CAS  Google Scholar 

  7. Sutherland FW et al. (2005) From stem cells to viable autologous semilunar heart valve. Circulation 111: 2783–2791

    Article  Google Scholar 

  8. Visconti RP et al. (2006) An in vivo analysis of hematopoietic stem cell potential: hematopoietic origin of cardiac valve interstitial cells. Circ Res 98: 690–696

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. RR Markwald is Distinguished University Professor and Chair of the Department of Anatomy and Cell Biology, and JT Butcher is a NRSA postdoctoral fellow jointly with the Department of Cell Biology and Pediatrics (Cardiology), and Director of the Cardiovascular Developmental Biology Centre, at the Medical University of South Carolina, Charleston, SC, USA.,

    Roger R Markwald & Jonathan T Butcher

Authors
  1. Roger R Markwald
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Jonathan T Butcher
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Roger R Markwald.

Ethics declarations

Competing interests

The authors declare no competing financial interests.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Markwald, R., Butcher, J. The next frontier in cardiovascular developmental biology—an integrated approach to adult disease?. Nat Rev Cardiol 4, 60–61 (2007). https://doi.org/10.1038/ncpcardio0775

Download citation

  • Received:

  • Accepted:

  • Issue Date:

  • DOI: https://doi.org/10.1038/ncpcardio0775

This article is cited by

Search

Advanced search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing