Evidence map›Paper›PMID 28064117›Full record

ArticleRedox biology2017

Differential proteomic and oxidative profiles unveil dysfunctional protein import to adipocyte mitochondria in obesity-associated aging and diabetes.

María Gómez-Serrano, Emilio Camafeita, Juan A López, Miguel A Rubio, Irene Bretón, Inés García-Consuegra, Eva García-Santos, Jesús Lago, Andrés Sánchez-Pernaute, Antonio Torres and 2 more

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Mitochondrial medicine in obesity: a scoping review.Open medicine (Warsaw, Poland) · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Mitochondrial Dysfunction in Diabetes: Shedding Light on a Widespread Oversight.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Review
  7. Article
  8. White adipose tissue mitochondrial bioenergetics in metabolic diseases.Reviews in endocrine & metabolic disorders · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Mitochondrial heterogeneity in diseases.Signal transduction and targeted therapy · 2023
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Pathways to Severe COVID-19 for People with Obesity.Obesity (Silver Spring, Md.) · 2021
    Review
  20. Article
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

12 authors at 6 institutions in 1 country.

María Gómez-SerranoInstituto de Investigaciones Biomédicas, Alberto Sols, (IIBM); Consejo Superior de Investigaciones Científicas & Universidad Autónoma de Madrid (CSIC-UAM), Madrid 28029, Spain.
Emilio CamafeitaLaboratory of Cardiovascular Proteomics, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid 28029, Spain.
Juan A LópezLaboratory of Cardiovascular Proteomics, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid 28029, Spain.
Miguel A RubioDepartment of Endocrinology, Hospital Clínico San Carlos (IDISSC), Facultad de Medicina, Universidad Complutense, Madrid 28040, Spain.
Irene BretónDepartment of Endocrinology and Nutrition, Hospital General Universitario Gregorio Marañón (IISGM), Madrid 28007, Spain.
Inés García-ConsuegraInstituto de Investigación, Hospital Universitario 12 de Octubre (i+12), Madrid 28041, Spain; Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), U723, Madrid 28029, Spain.
Eva García-SantosInstituto de Investigaciones Biomédicas, Alberto Sols, (IIBM); Consejo Superior de Investigaciones Científicas & Universidad Autónoma de Madrid (CSIC-UAM), Madrid 28029, Spain.
Jesús LagoDepartment of Surgery, Hospital General Universitario Gregorio Marañón (IISGM), Madrid 28007, Spain.
Andrés Sánchez-PernauteDepartment of Surgery, Hospital Clínico San Carlos (IDISSC), Facultad de Medicina, Universidad Complutense, Madrid 28040, Spain.
Antonio TorresDepartment of Surgery, Hospital Clínico San Carlos (IDISSC), Facultad de Medicina, Universidad Complutense, Madrid 28040, Spain.
Jesús VázquezLaboratory of Cardiovascular Proteomics, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid 28029, Spain.
Belén PeralInstituto de Investigaciones Biomédicas, Alberto Sols, (IIBM); Consejo Superior de Investigaciones Científicas & Universidad Autónoma de Madrid (CSIC-UAM), Madrid 28029, Spain. Electronic address: bperal@iib.uam.es.
Hospital Clínico San Carlos · ESSpanish National Centre for Cardiovascular Research · ESConsejo Superior de Investigaciones Científicas · ESHospital General Universitario Gregorio Marañón · ESHospital Universitario 12 De Octubre · ESUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human age-related diseases, including obesity and type 2 diabetes (T2DM), have long been associated to mitochondrial dysfunction; however, the role for adipose tissue mitochondria in these conditions remains unknown. We have tackled the impact of aging and T2DM on adipocyte mitochondria from obese patients by quantitating not only the corresponding abundance changes of proteins, but also the redox alterations undergone by Cys residues thereof. For that, we have resorted to a high-throughput proteomic approach based on isobaric labeling, liquid chromatography and mass spectrometry. The alterations undergone by the mitochondrial proteome revealed aging- and T2DM-specific hallmarks. Thus, while a global decrease of oxidative phosphorylation (OXPHOS) subunits was found in aging, the diabetic patients exhibited a reduction of specific OXPHOS complexes as well as an up-regulation of the anti-oxidant response. Under both conditions, evidence is shown for the first time of a link between increased thiol protein oxidation and decreased protein abundance in adipose tissue mitochondria. This association was stronger in T2DM, where OXPHOS mitochondrial- vs. nuclear-encoded protein modules were found altered, suggesting impaired mitochondrial protein translocation and complex assembly. The marked down-regulation of OXPHOS oxidized proteins and the alteration of oxidized Cys residues related to protein import through the redox-active MIA (Mitochondrial Intermembrane space Assembly) pathway support that defects in protein translocation to the mitochondria may be an important underlying mechanism for mitochondrial dysfunction in T2DM and physiological aging. The present draft of redox targets together with the quantification of protein and oxidative changes may help to better understand the role of oxidative stress in both a physiological process like aging and a pathological condition like T2DM.

Indexed as

AdipocytesAdultAgingDiabetes Mellitus, Type 2HumansMiddle AgedMitochondriaMitochondrial ProteinsObesityOxidation-ReductionOxidative PhosphorylationProtein TransportProteomeProteomicsSulfhydryl CompoundsMitochondrial ProteinsProteomeSulfhydryl CompoundsAdipose tissueMitochondriaOXPHOSRedox proteomicsThiol oxidationType 2 diabetes

Identifiers

PMID28064117
PMCPMC5220168
OpenAlexW2563002970

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.