Evidence map›Paper›PMID 32075490›Full record

ArticleJournal of the American Heart Association2020

Isha S Dhande, Yaming Zhu, Sterling C Kneedler, Aniket S Joshi, M John Hicks, Scott E Wenderfer, Michael C Braun, Peter A Doris

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Role of STIM1 in the Regulation of Cardiac Energy Substrate Preference.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Store-operated calcium entry: Pivotal roles in renal physiology and pathophysiology.Experimental biology and medicine (Maywood, N.J.) · 2021
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Journal of the American Heart Association · 2020
    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

8 authors at 3 institutions in 1 country.

Isha S DhandeInstitute of Molecular Medicine University of Texas Health Science Center at Houston Houston TX.
Yaming ZhuInstitute of Molecular Medicine University of Texas Health Science Center at Houston Houston TX.
Sterling C KneedlerInstitute of Molecular Medicine University of Texas Health Science Center at Houston Houston TX.
Aniket S JoshiInstitute of Molecular Medicine University of Texas Health Science Center at Houston Houston TX.
M John HicksDepartment of Pathology and Immunology Baylor College of Medicine and Texas Children's Hospital Houston TX.
Scott E WenderferDepartment of Pediatrics Baylor College of Medicine and Texas Children's Hospital Houston TX.
Michael C BraunDepartment of Pediatrics Baylor College of Medicine and Texas Children's Hospital Houston TX.
Peter A DorisInstitute of Molecular Medicine University of Texas Health Science Center at Houston Houston TX.
The University of Texas Health Science Center at Houston · USTexas Children's Hospital · USBaylor College of Medicine · US

Funding

Hypertensive Renal InjuryR01DK081866 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI DORIS, PETER A · 2009 to 2017
$2.9M
HNF1 transcriptional control of renal oxidative stressR01DK069632 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI DORIS, PETER A · 2005 to 2009
$1.4M
Immunogenetics of common polygenic renal diseaseR01DK114235 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI DORIS, PETER A · 2017 to 2020
$1.4M
NIDDK NIH HHS R01 DK069632NIDDK NIH HHS R01 DK081866NIDDK NIH HHS R01 DK114235
6 · The paper itself

Abstract

Background Spontaneously hypertensive rats of the stroke-prone line (SHR-A3) develop hypertensive renal disease as a result of naturally occurring genetic variation. Our prior work identified a single-nucleotide polymorphism unique to SHR-A3 that results in truncation of the carboxy terminus of STIM1. The SHR-B2 line, which is also hypertensive but resists hypertensive renal injury, expresses the wild-type STIM1. STIM1 plays a central role in lymphocyte calcium signaling that directs immune effector responses. Here we show that major defects in lymphocyte function affecting calcium signaling, nuclear factor of activated T cells activation, cytokine production, proliferation, apoptosis, and regulatory T-cell development are present in SHR-A3 and attributable to STIM1. Methods and Results To assess the role of

Indexed as

Lymphocyte ActivationPolymorphism, Single NucleotideAnimalsAntibody-Dependent Cell CytotoxicityAutoimmunityCalcium SignalingCD4-Positive T-LymphocytesCells, CulturedDisease Models, AnimalHypertensionKidneyKidney DiseasesMaleNFATC Transcription FactorsORAI1 ProteinRats, Inbred SHRNFATC Transcription FactorsORAI1 ProteinOrai1 protein, ratautoimmunityhypertensionimmunoglobulinrenal diseasespontaneously hypertensive rat

Identifiers

PMID32075490
PMCPMC7335582
OpenAlexW3006917209

What Socratic 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 Socratic graph.