Evidence map›Paper›PMID 19403643›Full record

ArticleAmerican journal of physiology. Renal physiology2009

Kidney ischemia-reperfusion injury induces caspase-dependent pulmonary apoptosis.

Heitham T Hassoun, Mihaela L Lie, Dmitry N Grigoryev, Manchang Liu, Rubin M Tuder, Hamid Rabb

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
4.6field-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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.

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2 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Heitham T HassounDepartment of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA. hhassou1@jhmi.edu
Mihaela L Lie
Dmitry N Grigoryev
Manchang Liu
Rubin M Tuder
Hamid Rabb
Johns Hopkins University · US

Funding

Sleep Related Mechanisms of COPD ProgressionP50HL084945 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI KRISHNAN, JERRY A. · 2007 to 2011
$15.1M
T Cell Modulation of Renal Ischemia Reperfusion InjuryR01DK054770 · NIDDK · MINNEAPOLIS MEDICAL RESEARCH FDN, INC. · PI RABB, HAMID · 2000 to 2009
$3.2M
Endothelial Cell Death in EmphysemaR01HL066554 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI TUDER, RUBIN M · 2000 to 2007
$2.6M
Biomakers in Sickle Cell Anemia: Response to HydroxyureaR01HL073944 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI STUART, MARIE J. · 2003 to 2004
$772k
Kidney-Lung interactions during ischemia-reperfusion injuryK08HL089181 · NHLBI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI HASSOUN, HEITHAM TALAL · 2008 to 2011
$542k
NHLBI NIH HHS K08 HL-089181NHLBI NIH HHS K08 HL089181NHLBI NIH HHS P50 HL-073944NHLBI NIH HHS P50-HL-084945NHLBI NIH HHS R01-HL-66554NIDDK NIH HHS R01 DK-54770
6 · The paper itself

Abstract

Distant organ effects of acute kidney injury (AKI) are a leading cause of morbidity and mortality. While little is known about the underlying mechanisms, limited data suggest a role for inflammation and apoptosis. Utilizing a lung candidate gene discovery approach in a mouse model of ischemic AKI-induced lung dysfunction, we identified prominent lung activation of 66 apoptosis-related genes at 6 and/or 36 h following ischemia, of which 6 genes represent the tumor necrosis factor receptor (TNFR) superfamily, and another 23 genes are associated with the TNFR pathway. Given that pulmonary apoptosis is an important pathogenic mechanism of acute lung injury (ALI), we hypothesized that AKI leads to pulmonary proapoptotic pathways that facilitate lung injury and inflammation. Functional correlation with 1) terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling and 2) active caspase-3 (aC3) activity, immunoblotting, and immunohistochemistry (IHC) identified kidney IRI-induced pulmonary apoptosis at 24 h, and colocalization studies with CD34 identified predominantly endothelial apoptosis. Mice were treated with the caspase inhibitor Z-VAD-FMK (0.25 mg ip) or vehicle 1 h before and 8 h after sham or kidney IRI, and bronchoalveolar lavage fluid protein was measured at 36 h as a surrogate for lung leak. Caspase inhibition reduced lung microvascular changes after kidney IRI. The pulmonary apoptosis seen in wild-type control mice during AKI was absent in TNFR(-/-) mice. Using an initial genomic approach to discovery followed by a mechanistic approach to disease targeting, we demonstrate that pulmonary endothelial apoptosis is a direct mediator of the distant organ dysfunction during experimental AKI.

Indexed as

Acute Kidney InjuryAcute Lung InjuryAmino Acid Chloromethyl KetonesAnimalsApoptosisCaspase 3Caspase InhibitorsDisease Models, AnimalEndotheliumGene Expression ProfilingLungMaleMiceMice, Inbred C57BLMice, KnockoutReceptors, Tumor Necrosis Factor, Type IAmino Acid Chloromethyl Ketonesbenzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketoneCaspase 3Caspase InhibitorsReceptors, Tumor Necrosis Factor, Type ITnfrsf1a protein, mouse

Identifiers

PMID19403643
PMCPMC2711715
OpenAlexW2101754323

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.