Evidence map›Paper›PMID 21270764›Full record

ArticleKidney international2011

Induction of heat shock protein 70 inhibits ischemic renal injury.

Zhiyong Wang, Jonathan M Gall, Ramon G B Bonegio, Andrea Havasi, Clayton R Hunt, Michael Y Sherman, John H Schwartz, Steven C Borkan

Open access · greenAbstract read
In one paragraph

Article in Kidney international, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.3field-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

51 citing papers in PubMed, 91 citations in OpenAlex.

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  16. Principles of Ice-Free Cryopreservation by Vitrification.Methods in molecular biology (Clifton, N.J.) · 2021
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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

8 authors at 3 institutions in 1 country.

Zhiyong WangRenal Section, Boston Medical Center, Evans Biomedical Research Center, Boston, Massachusetts 02118-2518, USA.
Jonathan M Gall
Ramon G B Bonegio
Andrea Havasi
Clayton R Hunt
Michael Y Sherman
John H Schwartz
Steven C Borkan
Boston Medical Center · USBoston University · USThe University of Texas Southwestern Medical Center · US

Funding

CYTOPROTECTIVE ROLE OF HSP72 IN RENAL CELL INJURYR01DK053387 · NIDDK · BOSTON MEDICAL CENTER · PI BORKAN, STEVEN C. · 1999 to 2016
$5.1M
MECHANISMS OF RENAL TUBULAR EPITHELIAL CELL INJURYR01DK052898 · NIDDK · BOSTON MEDICAL CENTER · PI SCHWARTZ, JOHN H · 1998 to 2005
$2.1M
Proteinuria causes progressive kidney disease by impairing autophagyK08DK090143 · NIDDK · BOSTON MEDICAL CENTER · PI HAVASI, ANDREA · 2011 to 2015
$746k
Tissue Sensitivity to Stress in The Absence of HSP70R03AG025286 · NIA · WASHINGTON UNIVERSITY · PI HUNT, CLAYTON R · 2005 to 2006
$136k
NIA NIH HHS AG025286NIA NIH HHS R03 AG025286NIDDK NIH HHS DK-52898NIDDK NIH HHS K08 DK090143NIDDK NIH HHS R01 DK052898NIDDK NIH HHS R01 DK053387NIDDK NIH HHS R0-1 DK-53387
6 · The paper itself

Abstract

Heat shock protein 70 (Hsp70) is a potent antiapoptotic agent. Here, we tested whether it directly regulates renal cell survival and organ function in a model of transient renal ischemia using Hsp70 knockout, heterozygous, and wild-type mice. The kidney cortical Hsp70 content inversely correlated with tubular injury, apoptosis, and organ dysfunction after injury. In knockout mice, ischemia caused changes in the activity of Akt and glycogen synthase kinase 3-β (kinases that regulate the proapoptotic protein Bax), increased active Bax, and activated the proapoptotic protease caspase 3. As these changes were significantly reduced in the wild-type mice, we tested whether Hsp70 influences ischemia-induced apoptosis. An Hsp70 inducer, geranylgeranylacetone, increased Hsp70 expression in heterozygous and wild-type mice, and reduced both ischemic tubular injury and organ dysfunction. When administered after ischemia, this inducer also decreased tubular injury and organ failure in wild-type mice but did not protect the knockout mice. ATP depletion in vitro caused greater mitochondrial Bax accumulation and death in primary proximal tubule cells harvested from knockout compared with wild-type mice and altered serine phosphorylation of a Bax peptide at the Akt-specific target site. In contrast, lentiviral-mediated Hsp70 repletion decreased mitochondrial Bax accumulation and rescued Hsp70 knockout cells from death. Thus, increasing Hsp70 either before or after ischemic injury preserves renal function by attenuating acute kidney injury.

Indexed as

Acute Kidney InjuryAnimalsApoptosisbcl-2-Associated X ProteinDiterpenesGene ExpressionGene Knockout TechniquesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHSP70 Heat-Shock ProteinsIschemiaKidneyMiceMice, Inbred C57BLMice, KnockoutProto-Oncogene ProteinsBax protein, mousebcl-2-Associated X ProteinBcl2 protein, mouseDiterpenesgeranylgeranylacetoneGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHSP70 Heat-Shock ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2Recombinant Proteins

Identifiers

PMID21270764
PMCPMC8006160
OpenAlexW1985209496

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.