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CD38/cyclic ADP-ribose signaling: role in the regulation of calcium homeostasis in airway smooth muscle

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00217.2004

Keywords

ryanodine receptor; calcium oscillations; inflammatory cytokines; muscarinic receptors; 12.6-kDa FK506-binding protein

Funding

  1. NHLBI NIH HHS [HL-55301, HL-057498, R01 HL057498, R01 HL064063, HL-64063, R01 HL055301] Funding Source: Medline
  2. NIDA NIH HHS [DA-11806, P50 DA011806] Funding Source: Medline

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The contractility of airway smooth muscle cells is dependent on dynamic changes in the concentration of intracellular calcium. Signaling molecules such as inositol 1,4,5-trisphosphate and cyclic ADP-ribose play pivotal roles in the control of intracellular calcium concentration. Alterations in the processes involved in the regulation of intracellular calcium concentration contribute to the pathogenesis of airway diseases such as asthma. Recent studies have identified cyclic ADP-ribose as a calcium-mobilizing second messenger in airway smooth muscle cells, and modulation of the pathway involved in its metabolism results in altered calcium homeostasis and may contribute to airway hyperresponsiveness. In this review, we describe the basic mechanisms underlying the dynamics of calcium regulation and the role of CD38/cADPR, a novel pathway, in the context of airway smooth muscle function and its contribution to airway diseases such as asthma.

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