Evidence map›Paper›PMID 27859269›Full record

ReviewJournal of cellular physiology2017

Homocysteine as a Pathological Biomarker for Bone Disease.

Jyotirmaya Behera, Jyoti Bala, Mohammed Nuru, Suresh C Tyagi, Neetu Tyagi

Open access · greenAbstract readReview
In one paragraph

Review in Journal of cellular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

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  18. Hormonal Changes in Women with Epilepsy.Neuropsychiatric disease and treatment · 2024
    Review
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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

5 authors at 1 institution in 1 country.

Jyotirmaya BeheraDepartment of Physiology, School of Medicine, University of Louisville, Louisville, Kentucky.
Jyoti BalaDepartment of Physiology, School of Medicine, University of Louisville, Louisville, Kentucky.
Mohammed NuruDepartment of Physiology, School of Medicine, University of Louisville, Louisville, Kentucky.
Suresh C TyagiDepartment of Physiology, School of Medicine, University of Louisville, Louisville, Kentucky.
Neetu TyagiDepartment of Physiology, School of Medicine, University of Louisville, Louisville, Kentucky.
University of Louisville · US

Funding

Mitigating mitochondrial epigenetics in bone remodeling by hydrogen sulfideR01AR067667 · NIAMS · UNIVERSITY OF LOUISVILLE · PI TYAGI, NEETU, TYAGI, SURESH C. · 2015 to 2019
$2.5M
Mechanisms of Mitochondrial Dysfunction in Brain VasculatureR01HL107640 · NHLBI · UNIVERSITY OF LOUISVILLE · PI TYAGI, NEETU · 2012 to 2016
$1.8M
NHLBI NIH HHS R01 HL107640NIAMS NIH HHS R01 AR067667
6 · The paper itself

Abstract

In the last few decades, perturbation in methyl-group and homocysteine (Hcy) balance have emerged as independent risk factors in a number of pathological conditions including neurodegenerative disease, cardiovascular dysfunction, cancer development, autoimmune disease, and kidney disease. Recent studies report Hcy to be a newly recognized risk factor for osteoporosis. Elevated Hcy levels are known to modulate osteoclastgenesis by causing detrimental effects on bone via oxidative stress induced metalloproteinase-mediated extracellular matrix degradation and decrease in bone blood flow. Evidence from previous studies also suggests that the decreased chondrocytes mediated bone mineralization in chick limb-bud mesenchymal cells and during the gestational period of ossification in rat model. However, Hcy imbalance and its role in bone loss, regression in vascular invasion, and osteoporosis, are not clearly understood. More investigations are required to explore the complex interplay between Hcy imbalance and onset of bone disease progression. This article reviews the current body of knowledge on regulation of Hcy mediated oxidative stress and its role in bone remodeling, vascular blood flow and progression of bone disease. J. Cell. Physiol. 232: 2704-2709, 2017. © 2016 Wiley Periodicals, Inc.

Indexed as

Bone RemodelingAnimalsBiomarkersBone and BonesChondrocytesCollagenDisease ProgressionHomocysteineHumansHyperhomocysteinemiaMatrix MetalloproteinasesMitochondriaOsteoclastsOsteogenesisOsteoporosisOxidative StressBiomarkersCollagenHomocysteineMatrix Metalloproteinases

Identifiers

PMID27859269
PMCPMC5576446
OpenAlexW2549903467

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.