Evidence map›Paper›PMID 25998388›Full record

ArticleBiochemical and biophysical research communications2015

Hemin activation of innate cellular response blocks human immunodeficiency virus type-1-induced osteoclastogenesis.

Kazuyo Takeda, Rewati Adhikari, Kenneth M Yamada, Subhash Dhawan

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Trial
  2. Dysregulated heme oxygenase-1Arthritis research & therapy · 2018
    Article
  3. Bone Loss in HIV Infection.Current treatment options in infectious diseases · 2017
    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

4 authors at 2 institutions in 1 country.

Kazuyo TakedaMicroscopy and Imaging Core Facility, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, MD, USA.
Rewati AdhikariDivision of Transfusion Transmitted Diseases, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD, USA.
Kenneth M YamadaNational Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA.
Subhash DhawanDivision of Transfusion Transmitted Diseases, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD, USA. Electronic address: subhash.dhawan@fda.hhs.gov.
Center for Biologics Evaluation and Research · USNational Institutes of Health · US

Funding

Craniofacial Developmental DynamicsZIADE000525 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI YAMADA, KENNETH · 2009 to 2025
$14.5M
Cell-Surface Interactions in PathogenesisZIADE000719 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI YAMADA, KENNETH · 2009 to 2025
$13.5M
Cell-Matrix Interactions and MigrationZIADE000524 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI YAMADA, KENNETH · 2009 to 2025
$10.2M
REGULATION OF CELL ADHESION, MIGRATION, AND MORPHOGENESISZ01DE000525 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI YAMADA, KENNETH MANAO · 1991 to 2008
$1.5M
INTEGRIN RECEPTOR FUNCTION AND SIGNALINGZ01DE000524 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI YAMADA, KENNETH MANAO · 1991 to 2008
$1.5M
Intramural FDA HHS FD999999Intramural NIH HHS Z01 DE000524Intramural NIH HHS Z01 DE000525Intramural NIH HHS Z99 DE999999
6 · The paper itself

Abstract

The normal skeletal developmental and homeostatic process termed osteoclastogenesis is exacerbated in numerous pathological conditions and causes excess bone loss. In cancer and HIV-1-infected patients, this disruption of homeostasis results in osteopenia and eventual osteoporesis. Counteracting the factors responsible for these metabolic disorders remains a challenge for preventing or minimizing this co-morbidity associated with these diseases. In this report, we demonstrate that a hemin-induced host protection mechanism not only suppresses HIV-1 associated osteoclastogenesis, but it also exhibits anti-osteoclastogenic activity for non-infected cells. Since the mode of action of hemin is both physiological and pharmacological through induction of heme oxygenase-1 (HO-1), an endogenous host protective response to an FDA-licensed therapeutic used to treat another disease, our study suggests an approach to developing novel, safe and effective therapeutic strategies for treating bone disorders, because hemin administration in humans has previously met required FDA safety standards.

Indexed as

Cell DifferentiationDrug ApprovalDrug RepositioningEnzyme InductionHeme Oxygenase-1HeminHIV-1HumansImmunity, InnateMacrophagesMonocytesOsteoclastsPrimary Cell CultureHeme Oxygenase-1HeminHMOX1 protein, humanHeme oxygenase-1HeminHIV-1Osteoclasts

Identifiers

PMID25998388
PMCPMC5260109
OpenAlexW290619986

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.