Regulators of G protein signaling in cardiovascular function during pregnancy

Abstract

G protein-coupled receptor signaling mechanisms are implicated in many aspects of cardiovascular control, and dysfunction of such signaling mechanisms is commonly associated with disease states. Investigators have identified a large number of regulator of G protein signaling (RGS) proteins that variously contribute to the modulation of intracellular second-messenger signaling kinetics. These many RGS proteins each interact with a specific set of second-messenger cascades and receptor types and exhibit tissue-specific expression patterns. Increasing evidence supports the contribution of RGS proteins, or their loss, in the pathogenesis of cardiovascular dysfunctions. This review summarizes the current understanding of the functional contributions of RGS proteins, particularly within the B/R4 family, in cardiovascular disorders of pregnancy including gestational hypertension, uterine artery dysfunction, and preeclampsia.

The renin–angiotensin system in the arcuate nucleus controls resting metabolic rate

“…Termination of G-protein signaling can be accelerated by Regulators of G-protein Signaling (RGS), which are GTPase activating proteins that function as endogenous terminators of G αi and G αq second-messenger signaling by increasing the intrinsic GTPase activity of G α subunits to facilitate the GTP-to-GDP exchange (55)(56)(57). Rgs2 is a potent suppressor of Agtr1a signaling in various cell types, and it is the dominant isoform expressed within Agrp neurons (37,58).…”

Crystal structure of human cysteamine dioxygenase provides a structural rationale for its function as an oxygen sensor

“…Dysregulation of either process would cause serious diseases, such as defects in oxidative stress, neurodegeneration, autoimmune, cardiovascular function, etc. (15)(16)(17)(18)(19) Consequently, ADO may be considered an emerging target for therapeutic intervention.…”

“…Hence, in addition to regulating thiol metabolism, ADO initiates a transduction cascade, signaling hypoxia and preserving oxygen homeostasis in humans. Dysregulation of either process would cause serious diseases, such as defects in oxidative stress, neurodegeneration, autoimmune, cardiovascular function, etc ( 15 , 16 , 17 , 18 , 19 ). Consequently, ADO may be considered an emerging target for therapeutic intervention.…”

Hypothalamic GPCR Signaling Pathways in Cardiometabolic Control

“…GPCR signal transduction can be regulated by Regulators of G-protein Signaling (RGS) proteins as well as β-arrestins. RGS proteins function as terminators of G protein signaling by enhancing the intrinsic GTPase activity of Gα subunits to facilitate the GTP to GDP hydrolysis, thereby promoting the reassociation between the G α and G α G α subunits ( Perschbacher et al, 2018 ). Thus, RGS proteins act to modulate the duration and subsequent termination of activated GPCR signaling.…”