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Editorial
. 2024 May 24;134(11):1402-1404.
doi: 10.1161/CIRCRESAHA.124.324574. Epub 2024 May 23.

New Kid on the Block: GLI1+ Cells and Pulmonary Arterioles Neomuscularization

Imad Al Ghouleh  1 , Andres Pulgarin Rocha  1 , Elena A Goncharova  2
Affiliations
Editorial

New Kid on the Block: GLI1+ Cells and Pulmonary Arterioles Neomuscularization

Imad Al Ghouleh et al. Circ Res. .
No abstract available

Keywords: Editorials; arterioles; hypoxia; pericytes; pulmonary artery.

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Conflict of interest statement

Disclosures None.

Figures

Figure.
Figure.. Various sources of de novo SMCs during distal vessels neo-muscularization in pulmonary hypertension.
New α-smooth muscle actin-positive (ACTA2+) cells in previously non-muscularized arterioles can originate from proliferation and downstream migration of proximal platelet-derived growth factor receptor-β-positive (PDGFR-β+) progenitor SMCs, which are positioned at the border of muscularized and non-muscularized pulmonary arterioles. Endothelial cells (ECs) can also contribute to this process via undergoing endothelial-to-mesenchymal transdifferentiation (EndMT). Resident lung PW1+ interstitial progenitor cells and their differentiation into SMC has also been reported. Pericytes can also give rise to SMCs contributing to distal vessel muscularization under hypoxia. Finally, GLI1+ mesenchymal cells have been newly identified to give rise to ACTA2+ SMCs and contribute to distal vessel muscularization.
See this image and copyright information in PMC

Comment on

  • GLI1+ Cells Contribute to Vascular Remodeling in Pulmonary Hypertension.
    Chu X, Kheirollahi V, Lingampally A, Chelladurai P, Valasarajan C, Vazquez-Armendariz AI, Hadzic S, Khadim A, Pak O, Rivetti S, Wilhelm J, Bartkuhn M, Crnkovic S, Moiseenko A, Heiner M, Kraut S, Atefi LS, Koepke J, Valente G, Ruppert C, Braun T, Samakovlis C, Alexopoulos I, Looso M, Chao CM, Herold S, Seeger W, Kwapiszewska G, Huang X, Zhang JS, Pullamsetti SS, Weissmann N, Li X, El Agha E, Bellusci S. Chu X, et al. Circ Res. 2024 May 24;134(11):e133-e149. doi: 10.1161/CIRCRESAHA.123.323736. Epub 2024 Apr 19. Circ Res. 2024. PMID: 38639105

References

    1. Mocumbi A, Humbert M, Saxena A, Jing ZC, Sliwa K, Thienemann F, Archer SL, Stewart S. Pulmonary hypertension. Nat Rev Dis Primers 2024; 10:5. - PubMed
    1. Gorelova A, Berman M, Al Ghouleh I. Endothelial-to-Mesenchymal Transition in Pulmonary Arterial Hypertension. Antioxid Redox Signal 2021; 34:891–914. - PMC - PubMed
    1. Farber HW, Loscalzo J. Pulmonary arterial hypertension. N Engl J Med 2004; 351:1655–1665. - PubMed
    1. Hislop A, Reid L. New findings in pulmonary arteries of rats with hypoxia-induced pulmonary hypertension. Br J Exp Pathol 1976; 57:542–554. - PMC - PubMed
    1. Sheikh AQ, Saddouk FZ, Ntokou A, Mazurek R, Greif DM. Cell Autonomous and Non-cell Autonomous Regulation of SMC Progenitors in Pulmonary Hypertension. Cell Rep 2018; 23:1152–1165. - PMC - PubMed

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