Evidence map›Paper›PMID 27398734›Full record

ReviewCanadian journal of physiology and pharmacology2017

Interactions of hyperhomocysteinemia and T cell immunity in causation of hypertension.

Sudhakar Veeranki, Siva K Gandhapudi, Suresh C Tyagi

Abstract readReview
In one paragraph

Review in Canadian journal of physiology and pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Review
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  14. Apolipoprotein E ε4/4 genotype limits response to dietary induction of hyperhomocysteinemia and resulting inflammatory signaling.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022
    Article
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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

3 authors at 1 institution in 1 country.

Sudhakar VeerankiDepartment of Physiology and Biophysics, Health Sciences Centre, A-1216, School of Medicine, University of Louisville, 500 South Pres Street, Louisville, KY, 40202, USA.
Siva K GandhapudiDepartment of Physiology and Biophysics, Health Sciences Centre, A-1216, School of Medicine, University of Louisville, 500 South Pres Street, Louisville, KY, 40202, USA.
Suresh C TyagiDepartment of Physiology and Biophysics, Health Sciences Centre, A-1216, School of Medicine, University of Louisville, 500 South Pres Street, Louisville, KY, 40202, USA.
University of Louisville · US

Funding

Reversing diabetic muscle myopathy by exercise and exosomesR01HL074185 · NHLBI · UNIVERSITY OF LOUISVILLE · PI TYAGI, SURESH C. · 2003 to 2018
$5.7M
Hydrogen sulfide mechanism of renal hypertensionR01DK104653 · NIDDK · UNIVERSITY OF LOUISVILLE · PI SEN, UTPAL, TYAGI, SURESH C. · 2015 to 2018
$2.5M
Mitophagic and anti-angiogenic mechanism of heart failureR01HL108621 · NHLBI · UNIVERSITY OF LOUISVILLE · PI TYAGI, SURESH C. · 2011 to 2015
$1.8M
NHLBI NIH HHS R01 HL074185NHLBI NIH HHS R01 HL108621NIDDK NIH HHS R01 DK104653
6 · The paper itself

Abstract

Although hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular diseases (CVD), there is a debate on whether HHcy is a risk factor or just a biomarker. Interestingly, homocysteine lowering strategies in humans had very little effect on reducing the cardiovascular risk, as compared with animals; this may suggest heterogeneity in human population and epigenetic alterations. Moreover, there are only few studies that suggest the idea that HHcy contributes to CVD in the presence of other risk factors such as inflammation, a known risk factor for CVD. Elevated levels of homocysteine have been shown to contribute to inflammation. Here, we highlight possible relationships between homocysteine, T cell immunity, and hypertension, and summarize the evidence that suggested these factors act together in increasing the risk for CVD. In light of this new evidence, we further propose that there is a need for evaluation of the causes of HHcy, defective remethylation or defective transsulfuration, which may differentially modulate hypertension progression, not just the homocysteine levels.

Indexed as

Blood PressureImmunity, CellularAnimalsBiomarkersHomocysteineHumansHyperhomocysteinemiaHypertensionInflammation MediatorsLymphocyte ActivationPrognosisRisk AssessmentRisk FactorsSignal TransductionT-LymphocytesUp-RegulationBiomarkersHomocysteineInflammation Mediatorscardiovascular diseasehyperhomocysteinemiahyperhomocystéinémiehypertensioninflammationlymphocytes Tmaladie cardiovasculaireT cells

Identifiers

PMID27398734
PMCPMC5519337
OpenAlexW2342781456

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.