Evidence map›Paper›PMID 35661621›Full record

ArticleJournal of molecular and cellular cardiology2022

Dual loss of regulator of G protein signaling 2 and 5 exacerbates ventricular myocyte arrhythmias and disrupts the fine-tuning of G

Shelby A Dahlen, Tyler F Bernadyn, Alethia J Dixon, Bo Sun, Jingsheng Xia, Elizabeth A Owens, Patrick Osei-Owusu

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 35% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. G protein regulation by RGS proteins in the pathophysiology of dilated cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  2. Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Shelby A DahlenDepartment of Physiology & Biophysics, Case Western Reserve University School of Medicine, Cleveland, OH 44106, United States of America.
Tyler F BernadynDepartment of Pharmacology & Physiology, Drexel University College of Medicine, Philadelphia, PA 19102, United States of America.
Alethia J DixonDepartment of Physiology & Biophysics, Case Western Reserve University School of Medicine, Cleveland, OH 44106, United States of America.
Bo SunDepartment of Physiology & Biophysics, Case Western Reserve University School of Medicine, Cleveland, OH 44106, United States of America.
Jingsheng XiaDepartment of Physiology & Biophysics, Case Western Reserve University School of Medicine, Cleveland, OH 44106, United States of America.
Elizabeth A OwensDepartment of Pharmacology & Physiology, Drexel University College of Medicine, Philadelphia, PA 19102, United States of America.
Patrick Osei-OwusuDepartment of Physiology & Biophysics, Case Western Reserve University School of Medicine, Cleveland, OH 44106, United States of America; Department of Pharmacology & Physiology, Drexel University College of Medicine, Philadelphia, PA 19102, United States of America. Electronic address: pxo70@case.edu.
Case Western Reserve University · USDrexel University · US

Funding

In Vivo Mechanisms of Integrated G protein Signaling Regulation by RGS ProteinsR01HL139754 · NHLBI · DREXEL UNIVERSITY · PI OSEI-OWUSU, PATRICK · 2018 to 2021
$1.6M
NHLBI NIH HHS R01 HL139754
6 · The paper itself

Abstract

aimsCardiac contractility, essential to maintaining proper cardiac output and circulation, is regulated by G protein-coupled receptor (GPCR) signaling. Previously, the absence of regulator of G protein signaling (RGS) 2 and 5, separately, was shown to cause G protein dysregulation, contributing to modest blood pressure elevation and exaggerated cardiac hypertrophic response to pressure-overload. Whether RGS2 and 5 redundantly control G protein signaling to maintain cardiovascular homeostasis is unknown. Here we examined how the dual absence of RGS2 and 5 (Rgs2/5 dbKO) affects blood pressure and cardiac structure and function. METHODS AND

resultsWe found that Rgs2/5 dbKO mice showed left ventricular dilatation at baseline by echocardiography. Cardiac contractile response to dobutamine stress test was sex-dependently reduced in male Rgs2/5 dbKO relative to WT mice. When subjected to surgery-induced stress, male Rgs2/5 dbKO mice had 75% mortality within 72-96 h after surgery, accompanied by elevated baseline blood pressure and decreased cardiac contractile function. At the cellular level, cardiomyocytes (CM) from Rgs2/5 dbKO mice showed augmented Ca

conclusionsWe conclude that RGS2 and 5 promote normal ventricular rhythm by coordinating their regulatory activity towards G

Indexed as

GTP-Binding Protein alpha Subunits, Gi-GoMyocytes, CardiacRGS ProteinsAnimalsArrhythmias, CardiacCardiomegalyMaleMiceSignal TransductionGTP-Binding Protein alpha Subunits, Gi-GoRgs2 protein, mouseRgs5 protein, mouseRGS ProteinsArrhythmiacAMPCardiac excitation-contraction couplingCardiomyopathyCatecholamineG protein signalingRGS proteins

Identifiers

PMID35661621
PMCPMC10211374
OpenAlexW4281980927

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.