Evidence map›Paper›PMID 21722304›Full record

ArticleJournal of cellular and molecular medicine2012

Type 2 diabetic obese db/db mice are refractory to myocardial ischaemic post-conditioning in vivo: potential role for Hsp20, F1-ATPase δ and Echs1.

Shu-Guang Zhu, Lei Xi, Rakesh C Kukreja

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 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

3 authors at 1 institution in 1 country.

Shu-Guang ZhuDivision of Cardiology, Department of Internal Medicine, VCU Pauley Heart Center, Virginia Commonwealth University, Richmond, VA 23298-0204, USA.
Lei Xi
Rakesh C Kukreja
Virginia Commonwealth University · US

Funding

Protection against Doxorubicin-Induced CardiomyopathyR37HL051045 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI KUKREJA, RAKESH C · 2006 to 2015
$3.8M
CARDIOPROTECTIVE EFFECTS OF PDE-5 INHIBITORSR01HL079424 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI KUKREJA, RAKESH C · 2005 to 2013
$3.6M
Cardioprotective Signaling following Phosphodiesterase-5 InhibitionR01HL093685 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI KUKREJA, RAKESH C · 2008 to 2012
$1.9M
SIGNALING MECHANISMS IN PHARMACOLOGICAL PRECONDITIONINGR01HL051045 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI KUKREJA, RAKESH C. · 1995 to 2004
$1.4M
NHLBI NIH HHS HL51045NHLBI NIH HHS HL79424NHLBI NIH HHS HL93685NHLBI NIH HHS R01 HL051045NHLBI NIH HHS R01 HL079424NHLBI NIH HHS R01 HL093685NHLBI NIH HHS R37 HL051045
6 · The paper itself

Abstract

Ischaemic post-conditioning (PostC) is a clinically relevant cardioprotective modality that has been confirmed in many species including human. It remains unknown if PostC can still protect heart in Type 2 diabetes, a rapidly growing disease in the world. This study investigated the efficacy of PostC in the leptin receptor-deficient db/db mice, which possess Type 2 diabetic characteristics including obesity, hyperglycaemia and hyperleptinaemia. Adult male C57BL/6J wild-type (WT) and db/db mice were anaesthetized, mechanically ventilated and subjected to left coronary artery occlusion for 30 min. followed by 24 hrs of reperfusion. For the PostC groups, the hearts underwent six cycles of 10 sec. of reperfusion and 10 sec. of re-occlusion at the onset of reperfusion. The mice were sacrificed at the end of 24 hrs reperfusion for infarct size measurement. PostC significantly reduced infarct size in WT mice (n = 6/group; P < 0.05), but not in the db/db mice. To identify alterations in protein expression by PostC, proteomic analyses were performed in the heart samples using two-dimensional differential in-gel electrophoresis with three CyDye labelling, followed by mass spectrometry. The results show that mitochondrial proteins (F(1)-ATPase γ and Echs1) were down-regulated by PostC in WT heart. Such change was absent in the db/db heart. On the other hand, PostC reduced Hsp20 in the diabetic heart. In summary, PostC fails to protect Type 2 diabetic mice against ischaemia-reperfusion injury. The potential protein targets for the loss of PostC may include F(1)-ATPase γ, Echs1 and Hsp20 that could regulate cellular ATP consumption/production and defense response to ischaemic stress.

Indexed as

AnimalsBlood GlucoseBody WeightDiabetes Mellitus, Type 2Enoyl-CoA HydrataseHSP20 Heat-Shock ProteinsMaleMiceMice, Inbred C57BLMitochondrial ProteinsMyocardial Reperfusion InjuryProton-Translocating ATPasesSpectrometry, Mass, Matrix-Assisted Laser Desorption-IonizationBlood GlucoseEnoyl-CoA HydrataseHSP20 Heat-Shock ProteinsMitochondrial ProteinsProton-Translocating ATPases

Identifiers

PMID21722304
PMCPMC3204159
OpenAlexW1990008701

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.