Evidence map›Paper›PMID 23554606›Full record

ArticleJournal of biomedical research2010

Emerging roles of cardiolipin remodeling in mitochondrial dysfunction associated with diabetes, obesity, and cardiovascular diseases.

Yuguang Shi

Open access · bronzeAbstract read
In one paragraph

Article in Journal of biomedical research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

64 citing papers in PubMed, 112 citations in OpenAlex.

  1. ALCAT1 promotes diabetic cardiomyopathy by linking myocardial tetralinoleoyl cardiolipin deficiency to lipotoxicity.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  2. Article
  3. Effects of Cannabidiol on TAFAZZIN-Deficient B-Lymphoblastoid Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Review
  5. Article
  6. Article
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  8. Article
  9. Review
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  11. Article
  12. Mitochondrial Dynamics and Insulin Secretion.International journal of molecular sciences · 2023
    Review
  13. Article
  14. Article
  15. The interplay of inflammation, exosomes and CaCardiovascular diabetology · 2023
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

4 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

1 author at 1 institution in 1 country.

Yuguang ShiDepartment of Cellular and Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, PA 17033, U.S.A.
Pennsylvania State University · US

Funding

Regulation of Mitochondrial Dysfunction in Diet-Induced Obesity by ALCAT-1R01DK076685 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI SHI, YUGUANG · 2008 to 2017
$2.8M
Regulation of Mitochondrial Dysfunction in Diet-Induced Obesity by ALCAT-1R56DK076685 · NIDDK · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI SHI, YUGUANG · 2007 to 2013
$228k
NIDDK NIH HHS R01 DK076685NIDDK NIH HHS R56 DK076685
6 · The paper itself

Abstract

Cardiolipin (CL) is a phospholipid exclusively localized in inner mitochondrial membrane where it is required for oxidative phosphorylation, ATP synthesis, and mitochondrial bioenergetics. The biological functions of CL are thought to depend on its acyl chain composition which is dominated by linoleic acids in metabolically active tissues. This unique feature is not derived from the de novo biosynthesis of CL, rather from a remodeling process that involves in phospholipases and transacylase/acyltransferase. The remodeling process is also believed to be responsible for generation of CL species that causes oxidative stress and mitochondrial dysfunction. CL is highly sensitive to oxidative damages by reactive oxygen species (ROS) due to its high content in polyunsaturated fatty acids and location near the site of ROS production. Consequently, pathological remodeling of CL has been implicated in the etiology of mitochondrial dysfunction commonly associated with diabetes, obesity, heart failure, neurodegeneration, and aging that are characterized by oxidative stress, CL deficiency, and abnormal CL species. This review summarizes recent progresses in molecular, enzymatic, lipidomic, and metabolic studies that support a critical regulatory role of pathological CL remodeling as a missing link between oxidative stress and mitochondrial dysfunction in metabolic diseases and aging.

Identifiers

PMID23554606
PMCPMC3596530
OpenAlexW2104816318

What Socratic holds

Textmetadata
LicenceCC BY
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.