Evidence map›Paper›PMID 27642497›Full record

ReviewOxidative medicine and cellular longevity2016

Cell Death and Heart Failure in Obesity: Role of Uncoupling Proteins.

Angélica Ruiz-Ramírez, Ocarol López-Acosta, Miguel Angel Barrios-Maya, Mohammed El-Hafidi

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  9. Uncoupling Proteins and Regulated Proton Leak in Mitochondria.International journal of molecular sciences · 2022
    Review
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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

4 authors at 1 institution in 1 country.

Angélica Ruiz-RamírezDepartamento de Biomedicina Cardiovascular, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano No. 1, Colonia Sección XVI, Tlalpan, 14080 Ciudad de México, DF, Mexico.
Ocarol López-AcostaDepartamento de Biomedicina Cardiovascular, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano No. 1, Colonia Sección XVI, Tlalpan, 14080 Ciudad de México, DF, Mexico.
Miguel Angel Barrios-MayaDepartamento de Biomedicina Cardiovascular, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano No. 1, Colonia Sección XVI, Tlalpan, 14080 Ciudad de México, DF, Mexico.
Mohammed El-HafidiDepartamento de Biomedicina Cardiovascular, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano No. 1, Colonia Sección XVI, Tlalpan, 14080 Ciudad de México, DF, Mexico.ORCID 0000-0002-5235-5642
Instituto Nacional de Cardiología · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic diseases such as obesity, metabolic syndrome, and type II diabetes are often characterized by increased reactive oxygen species (ROS) generation in mitochondrial respiratory complexes, associated with fat accumulation in cardiomyocytes, skeletal muscle, and hepatocytes. Several rodents studies showed that lipid accumulation in cardiac myocytes produces lipotoxicity that causes apoptosis and leads to heart failure, a dynamic pathological process. Meanwhile, several tissues including cardiac tissue develop an adaptive mechanism against oxidative stress and lipotoxicity by overexpressing uncoupling proteins (UCPs), specific mitochondrial membrane proteins. In heart from rodent and human with obesity, UCP2 and UCP3 may protect cardiomyocytes from death and from a state progressing to heart failure by downregulating programmed cell death. UCP activation may affect cytochrome c and proapoptotic protein release from mitochondria by reducing ROS generation and apoptotic cell death. Therefore the aim of this review is to discuss recent findings regarding the role that UCPs play in cardiomyocyte survival by protecting against ROS generation and maintaining bioenergetic metabolism homeostasis to promote heart protection.

Indexed as

Cell DeathCell SurvivalHeart FailureHumansLipid PeroxidationMitochondriaMitochondrial Uncoupling ProteinsMyocardiumReactive Oxygen SpeciesMitochondrial Uncoupling ProteinsReactive Oxygen Species

Identifiers

PMID27642497
PMCPMC5011521
OpenAlexW2507310498

What OpenQuestion 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 OpenQuestion graph.