CoChat
Sign Up
Cited by 169Tryptophan and brain disordersCardiac Health and Mental HealthAntioxidant Activity and Oxidative Stress

The DOI matches its Crossref record; 278 of the 288 references it cites were found in a registry or an index.

Multiple aberrations in shared inflammatory and oxidative & nitrosative stress (IO&NS) pathways explain the co-association of depression and cardiovascular disorder (CVD), and the increased risk for CVD and due mortality in depressed patients

Maes, Michael, Ruckoanich, Piyanuj, Chang, Young Seun, Mahanonda, Nithi, Berk, Michael·2011·Progress in Neuro-Psychopharmacology and Biological Psychiatry
DOI 10.1016/j.pnpbp.2010.06.008
Open this paper in CoChat — free account

Abstract

There is evidence that there is a bidirectional relationship between major depression and cardiovascular disorder (CVD): depressed patients are a population at risk for increased cardiac morbidity and mortality, and depression is more frequent in patients who suffer from CVD. There is also evidence that inflammatory and oxidative and nitrosative stress (IO&NS) pathways underpin the common pathophysiology of both CVD and major depression. Activation of these pathways may increase risk for both disorders and contribute to shared risk. The shared IO&NS pathways that may contribute to CVD and depression comprise the following: increased levels of pro-inflammatory cytokines, like interleukin-1β (IL-1β), IL-2, IL-6, IL-8, IL-12, tumor necrosis factor-α, and interferon-γ; T cell activation; increased acute phase proteins, like C-reactive protein, haptoglobin, fibrinogen and α1-antitrypsin; complement factors; increased LPS load through bacterial translocation and subsequent gut-derived inflammation; induction of indoleamine 2,3-dioxygenase with increased levels of tryptophan catabolites; decreased levels of antioxidants, like coenzyme Q10, zinc, vitamin E, glutathione and glutathione peroxidase; increased O&NS characterized by oxidative damage to low density lipoprotein (LDL) and phospholipid inositol, increased malondialdehyde, and damage to DNA and mitochondria; increased nitrosative stress; and decreased ω3 polyunsaturated fatty acids (PUFAs). The complex interplay between the abovementioned IO&NS pathways in depression results in pro-atherogenic effects and should be regarded as a risk factor to future clinical CVD and due mortality. We suggest that major depression should be added as a risk factor to the Charlson "comorbidity" index. It is advised that patients with (sub)chronic or recurrent major depression should routinely be assessed by serology tests to predict if they have an increased risk to cardiovascular disorders.

Overview

Integrity signals

Registry

Crossref · 10.1016/j.pnpbp.2010.06.008

Cites

278 of 278 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Research works printed but not linked: 2

  1. Maes, 1998, Fatty acids, cytokines, and major depression, Biol Psychiatry, 43, 313
  2. Maes, 2007, Neuro Endocrinol Lett, 28, 861

Cited by

Sorted by citations

See all 169

Related

See all

Metadata

Authors
Maes, M., Ruckoanich, P., Chang, Y. S., Mahanonda, N., & Berk, M.
Affiliations
  • Piyavate Hospital (TH)
  • Mental Health Research Institute (AU)
Corresponding author
Maes, Michael
ORCID
Venue
Progress in Neuro-Psychopharmacology and Biological Psychiatry
Publisher
Elsevier BV
Published
2011-04
Volume
35
Issue
3
Pages
769-783
ISSN
0278-5846 (ISSN-L)
DOI
10.1016/j.pnpbp.2010.06.008
OpenAlex
W2011854518
Cited by
169
References
288
Citations by year
2026: 4 · 2025: 17 · 2024: 10 · 2023: 9 · 2022: 8 · 2021: 7 · 2020: 13 · 2019: 10 · 2018: 9 · 2017: 10 · 2016: 13 · 2015: 15 · 2014: 12 · 2013: 12 · 2012: 12
FWCI
0.70
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Progress in Neuro-Psychopharmacology and Biological Psychiatry (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Health and Mental Health
  • Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
Keywords
major depressive disorder, cardiovascular disease, inflammatory signaling, oxidative stress, nitrosative stress, inflammatory cytokines, acute phase proteins, complement system, lipopolysaccharide, tryptophan catabolites, indoleamine 2,3-dioxygenase, antioxidants, atherosclerosis, omega-3 polyunsaturated fatty acids, cardiovascular mortality, Charlson Comorbidity Index
MeSH terms
Animals, Antioxidants, Cardiovascular Diseases, Depression, Female, Humans, Inflammation, Male, Risk, Fatty Acids, Omega-3, Nitrosation, Comorbidity, Oxidative Stress

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review