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May 22, 2022International Journal of Molecular SciencesOpen Access

Regulator of G-Protein Signaling-4 Attenuates Cardiac Adverse Remodeling and Neuronal Norepinephrine Release-Promoting Free Fatty Acid Receptor FFAR3 Signaling

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Why the study?

It was unknown whether regulator of G-protein signaling-4 modulates cardiac free fatty acid receptor-3 signaling and function.

Population

H9c2 cardiomyocytes and sympathetic-like neurons (differentiated Neuro-2a cells)

Comparison

siRNA-mediated RGS4 depletion and catecholamine pretreatment vs controls

Design

In vitro experimental cell study

Authors

ACAlexandra Marie CarboneUniversity of MiamiJBJordana I. BorgesNova Southeastern UniversityMSMalka S. SusterNova Southeastern University

Discussion

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Implication

RGS4 attenuates FFAR3-driven cardiac inflammation and fibrosis; leaves open its therapeutic targeting in AF.

Structured PICO

P
Population
H9c2 cardiomyocytes and sympathetic-like neurons (differentiated Neuro-2a cells)
I
Intervention
siRNA-mediated RGS4 depletion and catecholamine pretreatment
C
Comparator
Control cells (implied)
O
Outcome
Modulation of FFAR3 signaling (cAMP lowering, Gi/o activation, p38 MAPK activation, cytokine production, and norepinephrine release)surrogate

RGS4 is essential for attenuating propionate/FFAR3 signaling in cardiomyocytes and sympathetic neurons, protecting against inflammation and adverse remodeling.

Cite This Study

Carbone et al. (2022) studied this question.

synapsesocial.com/papers/6a70b30af44fa9f079de6343https://doi.org/10.3390/ijms23105803
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