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ABSTRACT: Background
Excess sodium intake induces vascular dysfunction. Molecular mechanisms underlying this are unclear. Here we investigated the role of reactive oxygen species (ROS), Ca2+ signaling and inflammation in salt-induced vascular injury, focusing on the interplay between redox-sensitive Poly(ADP-ribose) polymerase (PARP), which activates transient receptor potential melastatin 2 (TRPM2) Ca2+ channel, and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome. Specifically, we sought to determine if salt excess induces a pro-oxidant environment, leading to PARP-induced TRPM2 activation and increased Ca2+ influx, inflammasome assembly, and consequent vascular damage.Methods
Vascular smooth muscle cells (VSMCs) from rats and humans were expos
SUBMITTER: Alves-Lopes R
PROVIDER: S-EPMC12448623 | biostudies-literature | 2025 Sep
REPOSITORIES: biostudies-literature