Evidence map›Paper›PMID 28510229›Full record

ArticleBiophysical reviews2015

A change of heart: oxidative stress in governing muscle function?

Martin Breitkreuz, Nazha Hamdani

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

25 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. New Insight in Cardiorenal Syndrome: From Biomarkers to Therapy.International journal of molecular sciences · 2023
    Review
  6. Article
  7. Protein homeostasis in the aged and diseased heart.The journal of cardiovascular aging · 2023
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. The Role of Mitochondria in Metabolic Syndrome-Associated Cardiomyopathy.Oxidative medicine and cellular longevity · 2022
    Review
  13. Article
  14. Fundamental Mechanisms of the Cell Death Caused by Nitrosative Stress.Frontiers in cell and developmental biology · 2021
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. 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

2 authors at 1 institution in 1 country.

Martin BreitkreuzDepartment of Cardiovascular Physiology, Ruhr University Bochum, MA 3/56, 44780, Bochum, Germany.
Nazha HamdaniDepartment of Cardiovascular Physiology, Ruhr University Bochum, MA 3/56, 44780, Bochum, Germany. nazha.hamdani@rub.de.
Ruhr University Bochum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Redox/cysteine modification of proteins that regulate calcium cycling can affect contraction in striated muscles. Understanding the nature of these modifications would present the possibility of enhancing cardiac function through reversible cysteine modification of proteins, with potential therapeutic value in heart failure with diastolic dysfunction. Both heart failure and muscular dystrophy are characterized by abnormal redox balance and nitrosative stress. Recent evidence supports the synergistic role of oxidative stress and inflammation in the progression of heart failure with preserved ejection fraction, in concert with endothelial dysfunction and impaired nitric oxide-cyclic guanosine monophosphate-protein kinase G signalling via modification of the giant protein titin. Although antioxidant therapeutics in heart failure with diastolic dysfunction have no marked beneficial effects on the outcome of patients, it, however, remains critical to the understanding of the complex interactions of oxidative/nitrosative stress with pro-inflammatory mechanisms, metabolic dysfunction, and the redox modification of proteins characteristic of heart failure. These may highlight novel approaches to therapeutic strategies for heart failure with diastolic dysfunction. In this review, we provide an overview of oxidative stress and its effects on pathophysiological pathways. We describe the molecular mechanisms driving oxidative modification of proteins and subsequent effects on contractile function, and, finally, we discuss potential therapeutic opportunities for heart failure with diastolic dysfunction.

Indexed as

Contractile proteinsDiastolic stiffnessHeart failureOxidative stressPassive tensionPost-translational modificationsTitin

Identifiers

PMID28510229
PMCPMC5418422
OpenAlexW1007414750

What OpenQuestion holds

Textmetadata
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.