ArticleFrontiers in pharmacology2025
BAM8-22 targets spinal MrgC receptors to modulate UPR
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Bone cancer pain (BCP) significantly impacts patients' overall quality of life. Cellular energy metabolism homeostasis is critically dependent on mitochondrial integrity, and emerging evidence suggests that mitochondrial dysfunction in chronic BCP exacerbates pain progression by disrupting nociceptive signaling pathways. Notably, G protein-coupled receptors (GPCRs), a major class of membrane receptors, modulate mitochondrial function through diverse molecular mechanisms. In this study, we investigated the role of Mas-related G protein-coupled receptor C (MrgC) in BCP pathogenesis and its regulatory effects on mitochondrial function. Methods: Male C3H/HeN mice were utilized to establish a BCP model. Transmission electron microscopy and flow cytometry were employed to assess changes in mitochondrial ultrastructure, as well as levels of mtROS, ATP, and MMP in mice experiencing BCP. Following intrathecal injection of BAM8-22, we analyzed the effects of activated MrgC on mitochondrial unfolded protein response (UPR Results: Mice with bone cancer pain showed improved mRNA and protein levels of UPR Conclusion: By activating spinal MrgC to mediate UPR
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