Evidence map›Paper›PMID 28274939›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2017

Long-term HIF-1α transcriptional activation is essential for heat-acclimation-mediated cross tolerance: mitochondrial target genes.

Rivka Alexander-Shani, Ahmad Mreisat, Elia Smeir, Gary Gerstenblith, Michael D Stern, Michal Horowitz

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

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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

6 authors at 3 institutions in 2 countries.

Rivka Alexander-ShaniLaboratory of Environmental Physiology, Faculty of Dental Medicine, The Hebrew University, Jerusalem, Israel.
Ahmad MreisatLaboratory of Environmental Physiology, Faculty of Dental Medicine, The Hebrew University, Jerusalem, Israel.
Elia SmeirLaboratory of Environmental Physiology, Faculty of Dental Medicine, The Hebrew University, Jerusalem, Israel.
Gary GerstenblithCardiology, Johns Hopkins Hospital, Baltimore, Maryland; and.
Michael D SternGerontology Research Center, National Institute on Aging, Baltimore, Maryland.
Michal HorowitzLaboratory of Environmental Physiology, Faculty of Dental Medicine, The Hebrew University, Jerusalem, Israel; m.horowitz@mail.huji.ac.il.
Hebrew University of Jerusalem · ILJohns Hopkins Hospital · USNational Institute on Aging · US

Funding

Stochastic Simulation Of Excitation-contraction CouplingZIAAG000844 · NIA · NATIONAL INSTITUTE ON AGING · PI STERN, MICHAEL · 2009 to 2025
$8.7M
6 · The paper itself

Abstract

An important adaptive feature of heat acclimation (HA) is the induction of cross tolerance against novel stressors (HACT) Reprogramming of gene expression leading to enhanced innate cytoprotective features by attenuating damage and/or enhancing the response of "help" signals plays a pivotal role. Hypoxia-inducible factor-1α (HIF-1α), constitutively upregulated by HA (1 mo, 34°C), is a crucial transcription factor in this program, although its specific role is as yet unknown. By using a rat HA model, we studied the impact of disrupting HIF-1α transcriptional activation [HIF-1α:HIF-1β dimerization blockade by intraperitoneal acriflavine (4 mg/kg)] on its mitochondrial gene targets [phosphoinositide-dependent kinase-1 (PDK1), LON, and cyclooxygenase 4 (COX4) isoforms] in the HA rat heart. Physiological measures of cardiac HACT were infarct size after ischemia-reperfusion and time to rigor contracture during hypoxia in cardiomyocytes. We show that HACT requires transcriptional activation of HIF-1α throughout the course of HA and that this activation is accompanied by two metabolic switches:

Indexed as

AnimalsCells, CulturedHeat-Shock ProteinsHypoxia-Inducible Factor 1, alpha SubunitMaleMitochondria, HeartMitochondrial ProteinsMyocytes, CardiacRatsThermotoleranceTranscriptional ActivationTranscriptomeHeat-Shock ProteinsHif1a protein, ratHypoxia-Inducible Factor 1, alpha SubunitMitochondrial ProteinsacriflavineCOX4 isoformsheartheat acclimation-mediated cross toleranceHIF-1αPDK1

Identifiers

PMID28274939
PMCPMC5451574
OpenAlexW2593968479

What OpenQuestion holds

Textmetadata
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.