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Overview
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Background
Gadolinium chloride is a CaSR agonist. The CaSR can activate the NLRP3 inflammasome by increasing intracellular Ca2+ and decreasing cellular cyclic AMP. Thus, CaSR agonists may serve as a useful tool for exploring NLRP3 inflammasome associated inflammatory diseases such as cryopyrin-associated periodic syndromes, gout and atherosclerosis. In addition, gadolinium chloride has been demonstrated to block TRPML channel currents, as well as other transient receptor potential (TRP) channels.
1. Lee GS, Subramanian N, Kim AI, et al. The calcium-sensing receptor regulates the NLRP3 inflammasome through Ca2+ and cAMP. Nature, 2012, 492(7427): 123-127.
2. Nagata K, Zheng L, Madathany T, et al. The varitint-waddler (Va) deafness mutation in TRPML3 generates constitutive, inward rectifying currents and causes cell degeneration. Proceedings of the National Academy of Sciences of the United States of America, 2008, 105(1): 353-358.
3. Del Favero G, Florio C, Codan B, et al. The stretch-activated channel blocker Gd3+ reduces palytoxin toxicity in primary cultures of skeletal muscle cells. Chemical Research in Toxicology, 2012, 25(9): 1912-1920.
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