Korean J Physiol Pharmacol 2013 Feb; 17(1): 1-8
Amy L. Firth1,*, Jun Yeon Won2, and Won Sun Park3,*
Regulation of Ca2+ Signaling in Pulmonary Hypertension
1Laboratory of Genetics, Salk Institute for Biological Studies, La Jolla, California, USA, 2Department of Otolaryngology, Kangwon National University Hospital, School of Medicine, Kangwon National University, Chuncheon 200-722, 3Department of Physiology, School of Medicine, Kangwon National University, Chuncheon 200-701, Korea
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Understanding the cellular and molecular mechanisms involved in the development and progression of pulmonary hypertension (PH) remains imperative if we are to successfully improve the quality of life and life span of patients with the disease. A whole plethora of mechanisms are associated with the development and progression of PH. Such complexity makes it difficult to isolate one particular pathway to target clinically. Changes in intracellular free calcium concentration, the most common intracellular second messenger, can have significant impact in defining the pathogenic mechanisms leading to its development and persistence. Signaling pathways leading to the elevation of [Ca2+]cyt contribute to pulmonary vasoconstriction, excessive proliferation of smooth muscle cells and ultimately pulmonary vascular remodeling. This current review serves to summarize the some of the most recent advances in the regulation of calcium during pulmonary hypertension.

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