Evidence map›Paper›PMID 25188726›Full record

ReviewClinical pharmacology and therapeutics2014

Serendipity and the discovery of novel compounds that restore mitochondrial plasticity.

H H Szeto, A V Birk

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Clinical pharmacology and therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
6.1field-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

110 citing papers in PubMed, 189 citations in OpenAlex.

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  15. Mitochondria-Homing Drug Mitochonic Acid 5 Improves Barth Syndrome Myopathy in a Human-Induced Pluripotent Stem Cell Model and Barth Syndrome Drosophila Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  16. Article
  17. Contemporary insights into elamipretide's mitochondrial mechanism of action and therapeutic effects.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
    Review
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  19. Article
  20. Review

50 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.

H H SzetoResearch Program in Mitochondrial Therapeutics, Department of Pharmacology, Weill Cornell Medical College, New York, New York, USA.
A V BirkResearch Program in Mitochondrial Therapeutics, Department of Pharmacology, Weill Cornell Medical College, New York, New York, USA.
Cornell University · US

Funding

SPECIFICITY OF OXYGEN DNA DAMAGE AND MUTAGENESISP01AG001751 · NIA · UNIVERSITY OF WASHINGTON · PI MACCOSS, MICHAEL · 1985 to 2021
$29.6M
SYSTEMICALLY-ACTIVE OPIOID PEPTIDE ANALOGSP01DA008924 · NIDA · WEILL MEDICAL COLL OF CORNELL UNIV · PI DESIDERIO, DOMINIC M · 1994 to 2007
$6.5M
Cardiomyocyte mitochondria and mtROS in cardiac aging, hypertrophy and failureR01HL101186 · NHLBI · UNIVERSITY OF WASHINGTON · PI RABINOVITCH, PETER S · 2010 to 2013
$2.5M
Interrogating and manipulating mitochondrial ROS, energetics and proteomicsRC1AG035844 · NIA · UNIVERSITY OF WASHINGTON · PI RABINOVITCH, PETER S · 2009 to 2010
$505k
SS peptides: improve mitochondrial and skeletal muscle function with ageR21AG042637 · NIA · UNIVERSITY OF WASHINGTON · PI MARCINEK, DAVID J. · 2012 to 2013
$480k
Cell-Permeable Peptides for Mitochondrial ProtectionR21NS048295 · NINDS · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI SZETO, HAZEL H · 2004 to 2005
$389k
NHLBI NIH HHS HL-101186NHLBI NIH HHS R01 HL101186NIA NIH HHS AG-0001751NIA NIH HHS AG-042637NIA NIH HHS AG-35844NIA NIH HHS P01 AG001751NIA NIH HHS R21 AG042637NIA NIH HHS RC1 AG035844NIDA NIH HHS DA-08924NIDA NIH HHS P01 DA008924NINDS NIH HHS NS-048295NINDS NIH HHS R21 NS048295
6 · The paper itself

Abstract

The mitochondrial electron transport chain (ETC) plays a central role in energy generation in the cell. Mitochondrial dysfunctions diminish adenosine triphosphate (ATP) production and result in insufficient energy to maintain cell function. As energy output declines, the most energetic tissues are preferentially affected. To satisfy cellular energy demands, the mitochondrial ETC needs to be able to elevate its capacity to produce ATP at times of increased metabolic demand or decreased fuel supply. This mitochondrial plasticity is reduced in many age-associated diseases. In this review, we describe the serendipitous discovery of a novel class of compounds that selectively target cardiolipin on the inner mitochondrial membrane to optimize efficiency of the ETC and thereby restore cellular bioenergetics in aging and diverse disease models, without any effect on the normal healthy organism. The first of these compounds, SS-31, is currently in multiple clinical trials.

Indexed as

Drug DiscoveryAdenosine TriphosphateAgingBurnsCardiolipinsCytochromes cElectron TransportEnergy MetabolismHeart FailureHumansInsulin ResistanceMitochondriaMyocardial Reperfusion InjuryOligopeptidesAdenosine Triphosphatearginyl-2,'6'-dimethyltyrosyl-lysyl-phenylalaninamideCardiolipinsCytochromes cOligopeptides

Identifiers

PMID25188726
PMCPMC4267688
OpenAlexW2031535129

What Socratic 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 Socratic graph.