Evidence map›Paper›PMID 28384228›Full record

ArticlePloS one2017

Doxycycline protects against ROS-induced mitochondrial fragmentation and ISO-induced heart failure.

Adam Riba, Laszlo Deres, Krisztian Eros, Aliz Szabo, Klara Magyar, Balazs Sumegi, Kalman Toth, Robert Halmosi, Eszter Szabados

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.4field-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

33 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Salt and Gut Microbiota in Heart Failure.Current hypertension reports · 2023
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Doxycycline Decreases Atherosclerotic Lesions in the Aorta ofInternational journal of molecular sciences · 2022
    Article
  15. Article
  16. Article
  17. Review
  18. Effects of Shenfu Qiangxin Drink on HExperimental and therapeutic medicine · 2021
    Article
  19. Article
  20. New Targets in Heart Failure Drug Therapy.Frontiers in cardiovascular medicine · 2021
    Review
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

9 authors at 1 institution in 1 country.

Adam Riba1st Department of Medicine, University of Pecs, Pécs, Hungary.
Laszlo Deres1st Department of Medicine, University of Pecs, Pécs, Hungary.
Krisztian Eros1st Department of Medicine, University of Pecs, Pécs, Hungary.
Aliz SzaboDepartment of Biochemistry and Medical Chemistry, University of Pecs, Pécs, Hungary.
Klara Magyar1st Department of Medicine, University of Pecs, Pécs, Hungary.
Balazs SumegiSzentagothai ResearchCenter, University of Pecs, Pécs, Hungary.
Kalman Toth1st Department of Medicine, University of Pecs, Pécs, Hungary.
Robert Halmosi1st Department of Medicine, University of Pecs, Pécs, Hungary.
Eszter Szabados1st Department of Medicine, University of Pecs, Pécs, Hungary.
University of Pecs · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to their anti-bacterial action, tetracyclines also have complex biological effects, including the modification of mitochondrial protein synthesis, metabolism and gene-expression. Long-term clinical studies have been performed using tetracyclines, without significant side effects. Previous studies demonstrated that doxycycline (DOX), a major tetracyclin antibiotic, exerted a protective effect in animal models of heart failure; however, its exact molecular mechanism is still unknown. Here, we provide the first evidence that DOX reduces oxidative stress-induced mitochondrial fragmentation and depolarization in H9c2 cardiomyocytes and beneficially alters the expression of Mfn-2, OPA-1 and Drp-1 -the main regulators of mitochondrial fusion and fission-in our isoproterenol (ISO)-induced heart failure model, ultimately decreasing the severity of heart failure. In mitochondria, oxidative stress causes a shift toward fission which leads to mitochondrial fragmentation and cell death. Protecting mitochondria from oxidative stress, and the regulation of mitochondrial dynamics by drugs that shift the balance toward fusion, could be a novel therapeutic approach for heart failure. On the basis of our findings, we raise the possibility that DOX could be a novel therapeutic agent in the future treatment of heart failure.

Indexed as

Adrenergic beta-AgonistsAnimalsCell LineCollagenDoxycyclineHeart FailureIsoproterenolMaleMembrane Potential, MitochondrialMicroscopy, FluorescenceMitochondria, HeartMuscle ProteinsNatriuretic Peptide, BrainOxidative StressPhosphorylationRatsAdrenergic beta-AgonistsCollagenDoxycyclineIsoproterenolMuscle ProteinsNatriuretic Peptide, BrainReactive Oxygen Species

Identifiers

PMID28384228
PMCPMC5383248
OpenAlexW2604395177

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.