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Ann Thorac Surg 2009;88:424-425. doi:10.1016/j.athoracsur.2009.05.062
© 2009 The Society of Thoracic Surgeons
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Original Articles: General Thoracic

Invited Commentary

Thomas K. Waddell, MD, PhD

Division of Thoracic Surgery, Toronto General Hospital, 200 Elizabeth St, 9N-949, Toronto, Ontario, M5G 2C4, Canada

(Email: tom.waddell@uhn.on.ca).

The first 20% of the full text of this article appears below.

I read with interest the report by Yoshida and colleagues [1].

Cellular therapy for lung disease shows great promise, especially in the treatment of pulmonary arterial hypertension (PAH). Recent important advances have been made in our understanding both of the pathogenesis and treatment of this devastating disease. Gene hunting efforts in familial PAH have identified loss-of-function mutations in the bone morphogenetic protein-2 (BMP2) gene, a defect also seen in many patients with idiopathic PAH [2]. The BMP2 gene enhances resistance to inflammatory stress in both endothelial cells and circulating endothelial progenitors, an effect not seen in the circulating endothelial progenitor populations of PAH patients [3]. Heterozygous mutations . . . [Full Text of this Article]


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Syngeneic Bone Marrow Mononuclear Cells Improve Pulmonary Arterial Hypertension Through Vascular Endothelial Growth Factor Upregulation
Homare Yoshida, Takashi Kitaichi, Masahisa Urata, Hirotsugu Kurobe, Tamotsu Kanbara, Tatsuo Motoki, and Tetsuya Kitagawa
Ann. Thorac. Surg. 2009 88: 418-424. [Abstract] [Full Text] [PDF]





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