Evidence map›Paper›PMID 28804120›Full record

ReviewNature reviews. Nephrology2017

Mitochondrial energetics in the kidney.

Pallavi Bhargava, Rick G Schnellmann

Open access · bronzeAbstract readReview
In one paragraph

Review in Nature reviews. Nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 801 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
801citing papers in PubMed, 3 pooled it
25.5field-weighted citation impact, top 1% 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

801 citing papers in PubMed, 3 syntheses or guidelines pooled it, 1,243 citations in OpenAlex.

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741 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

2 authors at 1 institution in 1 country.

Pallavi BhargavaDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Drachman Hall, Room B307, 1295 N Martin Avenue, Tucson, Arizona 85721, USA.
Rick G SchnellmannDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Drachman Hall, Room B307, 1295 N Martin Avenue, Tucson, Arizona 85721, USA.
University of Arizona · US

Funding

Mitochondrial Biogenesis Promotes Recovery From Oxidant InjuryR01GM084147 · NIGMS · UNIVERSITY OF ARIZONA · PI SCHNELLMANN, RICK G · 2008 to 2016
$2.4M
Training in Bioenergetics, Oxidative Stress and Metabolic SyndromeT32DK083262 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LEMASTERS, JOHN J · 2009 to 2018
$1.5M
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 BX000851NIDDK NIH HHS T32 DK083262NIGMS NIH HHS R01 GM084147
6 · The paper itself

Abstract

The kidney requires a large number of mitochondria to remove waste from the blood and regulate fluid and electrolyte balance. Mitochondria provide the energy to drive these important functions and can adapt to different metabolic conditions through a number of signalling pathways (for example, mechanistic target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK) pathways) that activate the transcriptional co-activator peroxisome proliferator-activated receptor-γ co-activator 1α (PGC1α), and by balancing mitochondrial dynamics and energetics to maintain mitochondrial homeostasis. Mitochondrial dysfunction leads to a decrease in ATP production, alterations in cellular functions and structure, and the loss of renal function. Persistent mitochondrial dysfunction has a role in the early stages and progression of renal diseases, such as acute kidney injury (AKI) and diabetic nephropathy, as it disrupts mitochondrial homeostasis and thus normal kidney function. Improving mitochondrial homeostasis and function has the potential to restore renal function, and administering compounds that stimulate mitochondrial biogenesis can restore mitochondrial and renal function in mouse models of AKI and diabetes mellitus. Furthermore, inhibiting the fission protein dynamin 1-like protein (DRP1) might ameliorate ischaemic renal injury by blocking mitochondrial fission.

Indexed as

AnimalsDisease ProgressionHomeostasisHumansKidneyKidney DiseasesMitochondriaMitochondrial DiseasesSignal Transduction

Identifiers

PMID28804120
PMCPMC5965678
OpenAlexW2750514629

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.