Evidence mapPaperPMID 33545391Full record

ReviewMolecular metabolism2021

Therapeutic potential of mitochondrial uncouplers for the treatment of metabolic associated fatty liver disease and NASH.

Leigh Goedeke, Gerald I Shulman

Open access · goldAbstract readReview
In one paragraph

Review in Molecular metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
5.7field-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

45 citing papers in PubMed, 87 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

2 authors at 1 institution in 1 country.

Leigh GoedekeDepartment of Internal Medicine, Yale School of Medicine, New Haven, CT 06520, USA. Electronic address: leigh.goedeke@yale.edu.
Gerald I ShulmanDepartment of Internal Medicine, Yale School of Medicine, New Haven, CT 06520, USA; Department of Cellular and Molecular Physiology, Yale School of Medicine, New Haven, CT 06520, USA. Electronic address: gerald.shulman@yale.edu.
Yale University · US

Funding

Yale Liver CenterP30DK034989 · NIDDK · YALE UNIVERSITY · 1986 to 2025
$10.2M
Yale Diabetes Research CenterP30DK045735 · YALE UNIVERSITY · 1993 to 2025
$10.2M
Yale Clinical and Translational Science AwardUL1TR001863 · YALE UNIVERSITY · 2025 to 2025
$9.9M
Development of Controlled Release Mitochondrial Protonophore (CRMP) as a Novel Treatment for Type-2 Diabetes and Non-Alcoholic Steatohepatitis in Dysmetabolic Non-Human PrimatesR01DK119968 · NIDDK · YALE UNIVERSITY · PI GERALD I SHULMAN · 2023 to 2023
$532k
NCATS NIH HHS UL1 TR001863NHLBI NIH HHS K99 HL150234NIDDK NIH HHS P30 DK034989NIDDK NIH HHS P30 DK045735NIDDK NIH HHS R01 DK113984NIDDK NIH HHS R01 DK114793NIDDK NIH HHS R01 DK116774NIDDK NIH HHS R01 DK119968NIDDK NIH HHS RC2 DK120534
6 · The paper itself

Abstract

backgroundMitochondrial uncouplers shuttle protons across the inner mitochondrial membrane via a pathway that is independent of adenosine triphosphate (ATP) synthase, thereby uncoupling nutrient oxidation from ATP production and dissipating the proton gradient as heat. While initial toxicity concerns hindered their therapeutic development in the early 1930s, there has been increased interest in exploring the therapeutic potential of mitochondrial uncouplers for the treatment of metabolic diseases. SCOPE OF REVIEW: In this review, we cover recent advances in the mechanisms by which mitochondrial uncouplers regulate biological processes and disease, with a particular focus on metabolic associated fatty liver disease (MAFLD), nonalcoholic hepatosteatosis (NASH), insulin resistance, and type 2 diabetes (T2D). We also discuss the challenges that remain to be addressed before synthetic and natural mitochondrial uncouplers can successfully enter the clinic. MAJOR

conclusionsRodent and non-human primate studies suggest that a myriad of small molecule mitochondrial uncouplers can safely reverse MAFLD/NASH with a wide therapeutic index. Despite this, further characterization of the tissue- and cell-specific effects of mitochondrial uncouplers is needed. We propose targeting the dosing of mitochondrial uncouplers to specific tissues such as the liver and/or developing molecules with self-limiting properties to induce a subtle and sustained increase in mitochondrial inefficiency, thereby avoiding systemic toxicity concerns.

Indexed as

Adenosine TriphosphateAnimalsBiological ProductsDiabetes Mellitus, Type 2Fatty AcidsFatty LiverHumansInsulin ResistanceLiverLiver CirrhosisMetabolic SyndromeMitochondriaNon-alcoholic Fatty Liver DiseaseOxidation-ReductionAdenosine TriphosphateBiological ProductsFatty AcidsDiabetesInsulin resistanceLiver fibrosisMAFLDMetabolic syndromeMitochondrial uncouplersNAFLD/NASH

Identifiers

PMID33545391
PMCPMC8085597
OpenAlexW3127615859

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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 Socratic graph.