Evidence map›Paper›PMID 24834848›Full record

ReviewBiochimica et biophysica acta2015

Autophagy and oxidative stress in cardiovascular diseases.

Yu Mei, Melissa D Thompson, Richard A Cohen, XiaoYong Tong

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
15.0field-weighted citation impact, top 1% 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

104 citing papers in PubMed, 233 citations in OpenAlex.

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  13. Antioxidants: a comprehensive review.Archives of toxicology · 2025
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44 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

4 authors at 1 institution in 1 country.

Yu MeiVascular Biology Section, Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA.
Melissa D ThompsonVascular Biology Section, Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA.
Richard A CohenVascular Biology Section, Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA.
XiaoYong TongVascular Biology Section, Department of Medicine, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA 02118, USA. Electronic address: xytong@bu.edu.
Boston University · US

Funding

SIRT1, Polyphenols, and Endothelial OxidantsP01HL068758 · NHLBI · BOSTON MEDICAL CENTER · PI WALSH, KENNETH · 2003 to 2013
$14.1M
Redox Regulation of SERCA by Nitric OxideR01HL031607 · NHLBI · BOSTON UNIVERSITY MEDICAL CENTER HOSP · PI COHEN, RICHARD A · 1985 to 2013
$4.8M
Training Program in Cardiovascular Biology: Pre-DoctoralT32HL007969 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI RAVID, KATYA · 2003 to 2019
$3.2M
Redox Regulation of p21ras in AngiogenesisR37HL104017 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI COHEN, RICHARD A · 2010 to 2014
$2.2M
Aortic Stiffness and Hypertension in Obese MiceR01HL105287 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI COHEN, RICHARD A · 2010 to 2013
$1.6M
NHLBI NIH HHS HL031607NHLBI NIH HHS HL068758NHLBI NIH HHS HL07969NHLBI NIH HHS HL104017NHLBI NIH HHS HL105287NHLBI NIH HHS P01 HL068758NHLBI NIH HHS R01 HL031607NHLBI NIH HHS R01 HL105287NHLBI NIH HHS R37 HL104017NHLBI NIH HHS T32 HL007969
6 · The paper itself

Abstract

Autophagy is a highly conserved degradation process by which intracellular components, including soluble macromolecules (e.g. nucleic acids, proteins, carbohydrates, and lipids) and dysfunctional organelles (e.g. mitochondria, ribosomes, peroxisomes, and endoplasmic reticulum) are degraded by the lysosome. Autophagy is orchestrated by the autophagy related protein (Atg) composed protein complexes to form autophagosomes, which fuse with lysosomes to generate autolysosomes where the contents are degraded to provide energy for cell survival in response to environmental and cellular stress. Autophagy is an important player in cardiovascular disease development such as atherosclerosis, cardiac ischemia/reperfusion, cardiomyopathy, heart failure and hypertension. Autophagy in particular contributes to cardiac ischemia, hypertension and diabetes by interaction with reactive oxygen species generated in endoplasmic reticulum and mitochondria. This review highlights the dual role of autophagy in cardiovascular disease development. Full recognition of autophagy as an adaptive or maladaptive response would provide potential new strategies for cardiovascular disease prevention and management. This article is part of a Special Issue entitled: Autophagy and protein quality control in cardiometabolic diseases.

Indexed as

AutophagyOxidative StressAnimalsCardiovascular DiseasesHumansModels, BiologicalAtherosclerosisAutophagyCardiomyopathyHeart failureHypertensionOxidative stress

Identifiers

PMID24834848
PMCPMC4231019
OpenAlexW2065396708

What OpenQuestion 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 OpenQuestion graph.