Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comment
. 2019 Feb 21;176(5):947-949.
doi: 10.1016/j.cell.2019.01.053.

A Watershed Finding for Heart Regeneration

Affiliations
Comment

A Watershed Finding for Heart Regeneration

Evan S Bardot et al. Cell. .

Abstract

The adult mammalian heart is minimally regenerative after injury, whereas neonatal hearts fully recover even after major damage. New work from the Red-Horse and Woo labs (Das et al., 2019) shows that collateral artery formation is a key mechanism contributing to successful regeneration in newborn mice and provides insights into how collateral arteries form.

PubMed Disclaimer

Figures

Figure 1.
Figure 1.. Cxcr4/Cxcl12 Signaling Activates Arterial Endothelial Cells to Guide Collateral Artery Formation in Response to Myocardial Infarction
(A) Neonatal (P2) hearts subjected to left coronary artery ligation are able to restore blood flow to the injured region through the formation of collateral arteries by arterial reassembly. After the regenerative window (P7) hearts subjected to left coronary artery (LCA) ligation do not form collateral arteries. (B) Neonatal hearts lacking Cxcr4 in the arterial endothelial cells or Cxcl12 in the capillary bed are unable to recruit arterial endothelial cells (AECs) for arterial reassembly and form fibrotic scars after LCA ligation. Collateral artery reassembly is triggered by CXCL12-expressing capillaries, which activate and recruit CXCR4-expressing AECs to migrate, proliferate, and form new collateral arteries. (C)The injection of a high dose of CXCL12 rescues the formation of collateral arteries in P7 hearts.

Comment on

References

    1. Bassat E, Mutlak YE, Genzelinakh A, Shadrin IY, Baruch Umansky K, Yifa O, Kain D, Rajchman D, Leach J, Riabov Bassat D, et al. (2017). The extracellular matrix protein agrin promotes heart regeneration in mice. Nature 547, 179–184. - PMC - PubMed
    1. Cavallero S, Shen H, Yi C, Lien CL, Kumar SR, and Sucov HM (2015). CXCL12 Signaling Is Essential for Maturation of the Ventricular Coronary Endothelial Plexus and Establishment of Functional Coronary Circulation. Dev. Cell 33, 469–477. - PMC - PubMed
    1. Das S, Goldstone AB, Wang H, Farry J, D’Amato G, Paulsen MJ, Eskandari A, Hironaka CE, Phansalkar R, Sharma B, et al. (2019). A Unique Collateral Artery Development Program Promotes Neonatal Heart Regeneration. Cell 176, this issue, 1128–1142. - PMC - PubMed
    1. Goldstone AB, Burnett CE, Cohen JE, Paulsen MJ, Eskandari A, Edwards BE, Ingason AB, Steele AN, Patel JB, MacArthur JW, et al. (2018). SDF 1-alpha Attenuates Myocardial Injury Without Altering the Direct Contribution of Circulating Cells. J. Cardiovasc. Transl. Res. 11, 274–284. - PMC - PubMed
    1. Habib GB, Heibig J, Forman SA, Brown BG, Roberts R, Terrin ML, and Bolli R; The TIMI Investigators (1991). Influence of coronary collateral vessels on myocardial infarct size in humans. Results of phase I thrombolysis in myocardial infarction (TIMI) trial. Circulation 83, 739–746. - PubMed

Publication types

LinkOut - more resources