Title : Cystitis-Related Bladder Pain Involves ATP-Dependent HMGB1 Release from Macrophages and Its Downstream H2S/Cav3.2 Signaling in Mice.

Pub. Date : 2020 Jul 22

PMID : 32707767






2 Functional Relationships(s)
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1 The CPA-induced bladder pain was abolished by pharmacological inhibition of T-type Ca2+ channels or CSE, and genetic deletion of Cav3.2. Cyclophosphamide calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus
2 Together, our data suggest that CPA, once metabolized to acrolein, causes urothelial ATP-mediated, redox-dependent HMGB1 release from macrophages, which in turn causes RAGE-mediated CSE upregulation and subsequent H2S-targeted Cav3.2-dependent nociceptor excitation, resulting in bladder pain. Cyclophosphamide calcium channel, voltage-dependent, T type, alpha 1H subunit Mus musculus