Evidence map›Paper›PMID 24511124›Full record

ArticleJournal of the American Society of Nephrology : JASN2014

Formoterol restores mitochondrial and renal function after ischemia-reperfusion injury.

Sean R Jesinkey, Jason A Funk, L Jay Stallons, Lauren P Wills, Judit K Megyesi, Craig C Beeson, Rick G Schnellmann

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

97 citing papers in PubMed, 144 citations in OpenAlex.

  1. Norepinephrine regulates hippocampal mitochondrial biogenesis via β2-adrenergic receptor signaling and PGC-1α.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  8. Renal tubular epithelial IGFBP7 interacts with PKM2 to drive renal lipid accumulation and fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
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  15. βBiochemistry research international · 2025
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  16. Anthraquinones fromDrug design, development and therapy · 2025
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  20. Anti-adrenergic agents and the risk of postoperative acute kidney injury.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
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37 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

7 authors at 2 institutions in 1 country.

Sean R JesinkeyCenter for Cell Death, Injury, and Regeneration, Department of Drug Discovery and Biomedical Sciences, Medical University of South Carolina, Charleston, South Carolina;
Jason A FunkCenter for Cell Death, Injury, and Regeneration, Department of Drug Discovery and Biomedical Sciences, Medical University of South Carolina, Charleston, South Carolina;
L Jay StallonsCenter for Cell Death, Injury, and Regeneration, Department of Drug Discovery and Biomedical Sciences, Medical University of South Carolina, Charleston, South Carolina;
Lauren P WillsCenter for Cell Death, Injury, and Regeneration, Department of Drug Discovery and Biomedical Sciences, Medical University of South Carolina, Charleston, South Carolina;
Judit K MegyesiDepartment of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas; and.
Craig C BeesonCenter for Cell Death, Injury, and Regeneration, Department of Drug Discovery and Biomedical Sciences, Medical University of South Carolina, Charleston, South Carolina;
Rick G SchnellmannCenter for Cell Death, Injury, and Regeneration, Department of Drug Discovery and Biomedical Sciences, Medical University of South Carolina, Charleston, South Carolina; Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina.
Medical University of South Carolina · USUniversity of Arkansas for Medical Sciences · US

Funding

SOUTH CAROLINA COBRE IN OXIDANTS, REDOX BALANCE AND STRESS SIGNALINGP20GM103542 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BALL, LAUREN ELIZABETH · 2012 to 2020
$20.2M
TRAINING TO IMPROVE CARDIOVASCULAR THERAPIEST32HL007260 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI MENICK, DONALD R. · 1985 to 2021
$11.1M
SOUTH CAROLINA CLINICAL & TRANSLATIONAL RESEARCH INSTITUTE (SCTR)UL1RR029882 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T. · 2009 to 2011
$10.1M
Mitochondrial Biogenesis Promotes Recovery From Oxidant InjuryR01GM084147 · NIGMS · UNIVERSITY OF ARIZONA · PI SCHNELLMANN, RICK G · 2008 to 2016
$2.4M
MUSC FACIL EXPANSION &RENOV: SLE C06RR015455 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND, JOHN R · 2002 to 2002
$2.0M
TGF-beta1 and Mitochondrial Dysfunction in LPS-Induced Renal FailureF32DK098053 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI STALLONS, L. JAY · 2013 to 2013
$30k
5-HT Stimulation of Mitochondrial Biogenesis and Acute Kidney InjuryI01BX000851 · VA · SOUTHERN ARIZONA VA HEALTH CARE SYSTEM · PI SCHNELLMANN, RICK G · 2011 to 2025
–
BLRD VA I01 BX000851NCRR NIH HHS C06 RR015455NCRR NIH HHS UL1 RR029882NHLBI NIH HHS T32 HL007260NHLBI NIH HHS T32 HL007260-35NIDDK NIH HHS F32 DK098053NIDDK NIH HHS F32DK098053NIGMS NIH HHS P20 GM103542NIGMS NIH HHS P20 GM103542-02NIGMS NIH HHS R01 GM084147
6 · The paper itself

Abstract

Mitochondrial biogenesis may be an adaptive response necessary for meeting the increased metabolic and energy demands during organ recovery after acute injury, and renal mitochondrial dysfunction has been implicated in the pathogenesis of AKI. We proposed that stimulation of mitochondrial biogenesis 24 hours after ischemia/reperfusion (I/R)-induced AKI, when renal dysfunction is maximal, would accelerate recovery of mitochondrial and renal function in mice. We recently showed that formoterol, a potent, highly specific, and long-acting β2-adrenergic agonist, induces renal mitochondrial biogenesis in naive mice. Animals were subjected to sham or I/R-induced AKI, followed by once-daily intraperitoneal injection with vehicle or formoterol beginning 24 hours after surgery and continuing through 144 hours after surgery. Treatment with formoterol restored renal function, rescued renal tubules from injury, and diminished necrosis after I/R-induced AKI. Concomitantly, formoterol stimulated mitochondrial biogenesis and restored the expression and function of mitochondrial proteins. Taken together, these results provide proof of principle that a novel drug therapy to treat AKI, and potentially other acute organ failures, works by restoring mitochondrial function and accelerating the recovery of renal function after injury has occurred.

Indexed as

Acute Kidney InjuryAdrenergic beta-2 Receptor AgonistsAnimalsDisease Models, AnimalEnergy MetabolismEpithelial CellsEthanolaminesFormoterol FumarateKidneyKidney Tubules, ProximalMaleMiceMice, Inbred C57BLMitochondriaReperfusion InjuryAdrenergic beta-2 Receptor AgonistsEthanolaminesFormoterol Fumarateacute renal failureischemia-reperfusionmitochondriaproximal tubulerenal functionrenal tubular epithelial cells

Identifiers

PMID24511124
PMCPMC4033382
OpenAlexW2156449116

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.