Evidence map›Paper›PMID 26849408›Full record

ReviewAnnals of the New York Academy of Sciences2016

Atherogenesis: hyperhomocysteinemia interactions with LDL, macrophage function, paraoxonase 1, and exercise.

Ilya Chernyavskiy, Sudhakar Veeranki, Utpal Sen, Suresh C Tyagi

Abstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
5.4field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Homocysteine Attack on Vascular Endothelium-Old and New Features.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. The Relationship between Cancer and Paraoxonase 1.Antioxidants (Basel, Switzerland) · 2022
    Review
  10. Review
  11. Observational
  12. Article
  13. Article
  14. Oxidative Modifications in Advanced Atherosclerotic Plaques: A Focus onOxidative medicine and cellular longevity · 2020
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review
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

4 authors at 1 institution in 1 country.

Ilya ChernyavskiyDepartment of Physiology, University of Louisville, Louisville, Kentucky.
Sudhakar VeerankiDepartment of Physiology, University of Louisville, Louisville, Kentucky.
Utpal SenDepartment of Physiology, University of Louisville, Louisville, Kentucky.
Suresh C TyagiDepartment of Physiology, University of Louisville, Louisville, Kentucky.
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
Mechanism of Vascular Remodeling in HyperhomocysteinemiaR01HL071010 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI TYAGI, SURESH C. · 2002 to 2010
$2.7M
Mechanisms of Homocysteine-Induced Fibrinogen-Amyloid Plaque FormationR01NS084823 · NINDS · UNIVERSITY OF LOUISVILLE · PI LOMINADZE, DAVID, TYAGI, SURESH C. · 2013 to 2017
$2.7M
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 HL074185NHLBI NIH HHS HL108621NHLBI NIH HHS R01 HL071010NHLBI NIH HHS R01 HL074185NHLBI NIH HHS R01 HL108621NIDDK NIH HHS DK104653NIDDK NIH HHS R01 DK104653NINDS NIH HHS R01 NS084823
6 · The paper itself

Abstract

Despite great strides in understanding the atherogenesis process, the mechanisms are not entirely known. In addition to diet, cigarette smoking, genetic predisposition, and hypertension, hyperhomocysteinemia (HHcy), an accumulation of the noncoding sulfur-containing amino acid homocysteine (Hcy), is a significant contributor to atherogenesis. Although exercise decreases HHcy and increases longevity, the complete mechanism is unclear. In light of recent evidence, in this review, we focus on the effects of HHcy on macrophage function, differentiation, and polarization. Though there is need for further evidence, it is most likely that HHcy-mediated alterations in macrophage function are important contributors to atherogenesis, and HHcy-countering strategies, such as nutrition and exercise, should be included in the combinatorial regimens for effective prevention and regression of atherosclerotic plaques. Therefore, we also included a discussion on the effects of exercise on the HHcy-mediated atherogenic process.

Indexed as

ExerciseAnimalsAryldialkylphosphataseAtherosclerosisCholesterol, LDLDisease Models, AnimalDisease ProgressionHumansHyperhomocysteinemiaLipoproteins, LDLMacrophagesMiceOxidative StressPlaque, AtheroscleroticAryldialkylphosphataseCholesterol, LDLLipoproteins, LDLoxidized low density lipoproteinatherosclerosisexercisehyperhomocysteinemiamacrophageoxidized LDLPON1

Identifiers

PMID26849408
PMCPMC4801713
OpenAlexW2253642317

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.