Evidence map›Paper›PMID 25995211›Full record

ArticleCirculation. Arrhythmia and electrophysiology2015

Feedback mechanisms for cardiac-specific microRNAs and cAMP signaling in electrical remodeling.

Richard Myers, Valeriy Timofeyev, Ning Li, Catherine Kim, Hannah A Ledford, Padmini Sirish, Victor Lau, Yinuo Zhang, Kiran Fayyaz, Anil Singapuri and 4 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation. Arrhythmia and electrophysiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. miR-133: A Suppressor of Cardiac Remodeling?Frontiers in pharmacology · 2018
    Review
  10. Review
  11. Article
  12. 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

14 authors at 1 institution in 1 country.

Richard MyersFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (R.M., V.T.,N.L., C.K., H.A.L., P.S., V.L., Y.Z., K.F., A.S., J.E.L., A.A.K., X.-D.Z., N.C.); and Department of Veterans Affairs, Northern California Health Care System, Mather (A.A.K., N.C.).
Valeriy TimofeyevFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (R.M., V.T.,N.L., C.K., H.A.L., P.S., V.L., Y.Z., K.F., A.S., J.E.L., A.A.K., X.-D.Z., N.C.); and Department of Veterans Affairs, Northern California Health Care System, Mather (A.A.K., N.C.).
Ning LiFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (R.M., V.T.,N.L., C.K., H.A.L., P.S., V.L., Y.Z., K.F., A.S., J.E.L., A.A.K., X.-D.Z., N.C.); and Department of Veterans Affairs, Northern California Health Care System, Mather (A.A.K., N.C.).
Catherine KimFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (R.M., V.T.,N.L., C.K., H.A.L., P.S., V.L., Y.Z., K.F., A.S., J.E.L., A.A.K., X.-D.Z., N.C.); and Department of Veterans Affairs, Northern California Health Care System, Mather (A.A.K., N.C.).
Hannah A LedfordFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (R.M., V.T.,N.L., C.K., H.A.L., P.S., V.L., Y.Z., K.F., A.S., J.E.L., A.A.K., X.-D.Z., N.C.); and Department of Veterans Affairs, Northern California Health Care System, Mather (A.A.K., N.C.).
Padmini SirishFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (R.M., V.T.,N.L., C.K., H.A.L., P.S., V.L., Y.Z., K.F., A.S., J.E.L., A.A.K., X.-D.Z., N.C.); and Department of Veterans Affairs, Northern California Health Care System, Mather (A.A.K., N.C.).
Victor LauFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (R.M., V.T.,N.L., C.K., H.A.L., P.S., V.L., Y.Z., K.F., A.S., J.E.L., A.A.K., X.-D.Z., N.C.); and Department of Veterans Affairs, Northern California Health Care System, Mather (A.A.K., N.C.).
Yinuo ZhangFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (R.M., V.T.,N.L., C.K., H.A.L., P.S., V.L., Y.Z., K.F., A.S., J.E.L., A.A.K., X.-D.Z., N.C.); and Department of Veterans Affairs, Northern California Health Care System, Mather (A.A.K., N.C.).
Kiran FayyazFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (R.M., V.T.,N.L., C.K., H.A.L., P.S., V.L., Y.Z., K.F., A.S., J.E.L., A.A.K., X.-D.Z., N.C.); and Department of Veterans Affairs, Northern California Health Care System, Mather (A.A.K., N.C.).
Anil SingapuriFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (R.M., V.T.,N.L., C.K., H.A.L., P.S., V.L., Y.Z., K.F., A.S., J.E.L., A.A.K., X.-D.Z., N.C.); and Department of Veterans Affairs, Northern California Health Care System, Mather (A.A.K., N.C.).
Javier E LopezFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (R.M., V.T.,N.L., C.K., H.A.L., P.S., V.L., Y.Z., K.F., A.S., J.E.L., A.A.K., X.-D.Z., N.C.); and Department of Veterans Affairs, Northern California Health Care System, Mather (A.A.K., N.C.).
Anne A KnowltonFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (R.M., V.T.,N.L., C.K., H.A.L., P.S., V.L., Y.Z., K.F., A.S., J.E.L., A.A.K., X.-D.Z., N.C.); and Department of Veterans Affairs, Northern California Health Care System, Mather (A.A.K., N.C.).
Xiao-Dong ZhangFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (R.M., V.T.,N.L., C.K., H.A.L., P.S., V.L., Y.Z., K.F., A.S., J.E.L., A.A.K., X.-D.Z., N.C.); and Department of Veterans Affairs, Northern California Health Care System, Mather (A.A.K., N.C.). nchiamvimonvat@ucdavis.edu xdzhang@ucdavis.edu.
Nipavan ChiamvimonvatFrom the Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis (R.M., V.T.,N.L., C.K., H.A.L., P.S., V.L., Y.Z., K.F., A.S., J.E.L., A.A.K., X.-D.Z., N.C.); and Department of Veterans Affairs, Northern California Health Care System, Mather (A.A.K., N.C.). nchiamvimonvat@ucdavis.edu xdzhang@ucdavis.edu.
Anna Needs Neuroblastoma Answers · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WILLIAM H HERMAN · 2013 to 2026
$24.3M
UC Davis Clinical and Translational Science CenterUL1TR000002 · NCATS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERGLUND, LARS F · 2012 to 2015
$12.2M
Functional Interactions of Cardiac Ion ChannelsR01HL085844 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN · 2007 to 2025
$7.3M
Training Program In Basic & Translational Cardiovascular ScienceT32HL086350 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Martin Cadeiras, David A. Liem · 2008 to 2026
$7.1M
Translational Study of Cardiac DysfunctionR01HL085727 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN, SIRISH, PADMINI · 2008 to 2022
$5.7M
Human Cardiomyopathy and HSP60R01HL077281 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI KNOWLTON, ANNE A · 2004 to 2012
$3.1M
HSPs, Inflammatory Response and Cardiovascular DiseaseR01HL079071 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI KNOWLTON, ANNE A · 2006 to 2014
$2.7M
Decoding the enigma of cardiac amplificationR01HL137228 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN · 2017 to 2020
$2.2M
Functions of calcium-activated ion channels in the heartR01HL075274 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI CHIAMVIMONVAT, NIPAVAN · 2004 to 2007
$1.5M
In Vivo Ultrasound Imaging System (VEVO 2100, VisualSonics)S10OD010389 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN · 2013 to 2013
$397k
Regulation of ion channels in the heartI01BX000576 · VA · VA NORTHERN CALIFORNIA HEALTH CARE SYS · PI CHIAMVIMONVAT, NIPAVAN · 2009 to 2019
–
Estrogen, Aging and Vascular InflammationI01BX000839 · VA · VA NORTHERN CALIFORNIA HEALTH CARE SYS · PI KNOWLTON, ANNE A · 2011 to 2014
–
BLRD VA I01 BX000576BLRD VA I01 BX000839CSRD VA I01 CX001490NCATS NIH HHS UL1 TR000002NCRR NIH HHS S10 RR033106NHLBI NIH HHS R01 HL075274NHLBI NIH HHS R01 HL077281NHLBI NIH HHS R01 HL079071NHLBI NIH HHS R01 HL085727NHLBI NIH HHS R01 HL085844NHLBI NIH HHS R01 HL137228NHLBI NIH HHS T32 HL086350NHLBI NIH HHS T32 NIH HL086350NIDDK NIH HHS P30 DK020572NIH HHS S10 OD010389
6 · The paper itself

Abstract

backgroundLoss of transient outward K(+) current (Ito) is well documented in cardiac hypertrophy and failure both in animal models and in humans. Electrical remodeling contributes to prolonged action potential duration and increased incidence of arrhythmias. Furthermore, there is a growing body of evidence linking microRNA (miR) dysregulation to the progression of both conditions. In this study, we examined the mechanistic basis underlying miR dysregulation in electrical remodeling and revealed a novel interaction with the adrenergic signaling pathway. METHODS AND

resultsWe first used a tissue-specific knockout model of Dicer1 in cardiomyocytes to reveal the overall regulatory effect of miRs on the ionic currents and action potentials. We then validated the inducible cAMP early repressor as a target of miR-1 and took advantage of a clinically relevant model of post myocardial infarction and miR delivery to probe the mechanistic basis of miR dysregulation in electrical remodeling. These experiments revealed the role of inducible cAMP early repressor as a repressor of miR-1 and Ito, leading to prolonged action potential duration post myocardial infarction. In addition, delivery of miR-1 and miR-133a suppressed inducible cAMP early repressor expression and prevented both electrical remodeling and hypertrophy.

conclusionsTaken together, our results illuminate the mechanistic links between miRs, adrenergic signaling, and electrical remodeling. They also serve as a proof-of-concept for the therapeutic potential of miR delivery post myocardial infarction.

Indexed as

Gene Expression RegulationAnimalsAnimals, NewbornAtrial RemodelingBlotting, WesternCardiomegalyCells, CulturedCyclic AMPDEAD-box RNA HelicasesDisease Models, AnimalFlow CytometryMiceMice, Inbred C57BLMicroRNAsMyocardiumMyocytes, CardiacCyclic AMPDEAD-box RNA HelicasesDicer1 protein, mouseMicroRNAsRibonuclease IIIcAMPelectrical remodelingion channelmicroRNAmyocardial infarction

Identifiers

PMID25995211
PMCPMC4545299
OpenAlexW2294212678

What OpenQuestion holds

Textmetadata
LicenceTDM
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.