The three R’s of lung health and disease: repair, remodeling, and regeneration
Michael F. Beers, Edward E. Morrisey
Michael F. Beers, Edward E. Morrisey
Published June 1, 2011
Citation Information: J Clin Invest. 2011;121(6):2065-2073. https://doi.org/10.1172/JCI45961.
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The three R’s of lung health and disease: repair, remodeling, and regeneration

Abstract

All tissues and organs can be classified according to their ability to repair and regenerate during adult homeostasis and after injury. Some exhibit a high rate of constant cell turnover, while others, such as the lung, exhibit only low-level cell regeneration during normal adult homeostasis but have the ability to rapidly regenerate new cells after injury. Lung regeneration likely involves both activation of progenitor cells as well as cell replacement through proliferation of remaining undamaged cells. The pathways and factors that control this process and its role in disease are only now being explored. In this Review, we will discuss the connection between pathways required for lung development and how the lung responds to injury and disease, with a particular emphasis on recent studies describing the role for the epithelium in repair and regeneration.

Authors

Michael F. Beers, Edward E. Morrisey

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Figure 1

Early patterning and morphogenesis of the anterior foregut and origin of epithelial cell lineages in the lung.

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Early patterning and morphogenesis of the anterior foregut and origin of...
(A) Diagram of the early anterior foregut development, showing the relationship between Wnt2/2b and Fgf10, which are expressed in the early ventral anterior mesoderm surrounding the foregut. Wnt2/2b act upstream of Fgf10 (and other factors including Bmp4) to induce lung specification in the most ventral aspect of the anterior foregut endoderm, as noted by expression of Nkx2.1. (B) As lung development ensues, the endoderm goes through extensive and reiterated branching, setting up the proximal-distal patterning of the airways. This results in distinct progenitors located within the proximal (Sox2+) and distal (Sox9, Id2, Foxp2) airway epithelium. However, the distal Id2+ progenitors can generate proximal epithelium up to E13.5 of mouse development (B, arrows) (6).