Evidence map›Paper›PMID 31258063›Full record

ArticleCurrent pharmaceutical design2019

The Role of Autophagy and Death Pathways in Dose-dependent Isoproterenolinduced Cardiotoxicity.

Alexandra Gyongyosi, Rita Zilinyi, Andras Czegledi, Agnes Tosaki, Arpad Tosaki, Istvan Lekli

Abstract read
In one paragraph

Article in Current pharmaceutical design, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Protective Effects of 2-Methoxyestradiol on Acute Isoproterenol-Induced Cardiac Injury in Rats.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
    Article
  3. Autophagy in Heart Failure: Insights into Mechanisms and Therapeutic Implications.Journal of cardiovascular development and disease · 2023
    Review
  4. Article
  5. Cardioprotective Activity ofEvidence-based complementary and alternative medicine : eCAM · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. ArrhythmoGenoPharmacoTherapy.Frontiers in pharmacology · 2020
    Review
  12. Article
  13. 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

6 authors.

Alexandra GyongyosiDepartment of Pharmacology, Faculty of Pharmacy, University of Debrecen, Debrecen, Hungary.
Rita ZilinyiDepartment of Pharmacology, Faculty of Pharmacy, University of Debrecen, Debrecen, Hungary.
Andras CzeglediDepartment of Pharmacology, Faculty of Pharmacy, University of Debrecen, Debrecen, Hungary.
Agnes TosakiDepartment of Dermatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Arpad TosakiDepartment of Pharmacology, Faculty of Pharmacy, University of Debrecen, Debrecen, Hungary.
Istvan LekliDepartment of Pharmacology, Faculty of Pharmacy, University of Debrecen, Debrecen, Hungary.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIsoproterenol (ISO) is a non-selective β-adrenergic agonist. Our aims were to investigate the autophagy and cell death pathways including apoptosis and necrosis in ISO-induced cardiac injury in a dosedependent manner.

methodsMale Sprague-Dawley rats were treated for 24 hours with I. vehicle (saline); II. 0.005 mg/kg ISO; III. 0.05 mg/kg ISO; IV. 0.5 mg/kg ISO; V. 5 mg/kg ISO; VI. 50 mg/kg ISO, respectively. Hearts were isolated and infarct size was measured. Serum levels of Troponin T (TrT), lactate dehydrogenase (LDH), creatine kinase isoenzyme MB (CK-MB) were measured. TUNEL assay was carried out to monitor apoptotic cell death and Western blot was performed to evaluate the level of autophagic and apoptotic markers.

resultsSurvival rate of animals was dose-dependently decreased by ISO. Serum markers and infarct size revealed the development of cardiac toxicity. Level of Caspase-3, and results of TUNEL assay, demonstrated that the level of apoptosis was dose-dependently increased. They reached the highest level in ISO 5 and it decreased slightly in ISO 50 group. Focusing on autophagic proteins, we found that level of Beclin-1 was increased in a dose-dependent manner, but significantly increased in ISO 50 treated group. Level of LC3B-II and p62 showed the same manner, but the elevated level of p62 indicated that autophagy was impaired in both ISO 5 and ISO 50 groups.

conclusionTaken together these results suggest that at smaller dose of ISO autophagy may cope with the toxic effect of ISO; however, at higher dose apoptosis is initiated and at the highest dose substantial necrosis occurs.

Indexed as

ApoptosisAutophagyCardiotoxicityAnimalsHeartIsoproterenolMaleMyocardiumRatsRats, Sprague-DawleyIsoproterenolapoptosisautophagycardiotoxicityIsoproterenolnecrosisβ-adrenergic agonist.

Identifiers

PMID31258063
PMCPMC6806536

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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.