Evidence map›Paper›PMID 33088945›Full record

ArticleHeliyon2020

Activation of SIRT1/PGC 1α/SIRT3 pathway by melatonin provides protection against mitochondrial dysfunction in isoproterenol induced myocardial injury.

Shamreen Naaz, Sanatan Mishra, Palash K Pal, Aindrila Chattopadhyay, Asish R Das, Debasish Bandyopadhyay

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Heliyon, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

26 citing papers in PubMed, 37 citations in OpenAlex.

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  20. Hepatic Encephalopathy and Melatonin.Antioxidants (Basel, Switzerland) · 2022
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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 at 2 institutions in 1 country.

Shamreen NaazDepartment of Physiology, Oxidative Stress and Free Radical Biology Laboratory, University of Calcutta, University College of Science and Technology, 92, APC Road, Kolkata 700 009, West Bengal, India.
Sanatan MishraDepartment of Physiology, Oxidative Stress and Free Radical Biology Laboratory, University of Calcutta, University College of Science and Technology, 92, APC Road, Kolkata 700 009, West Bengal, India.
Palash K PalDepartment of Physiology, Oxidative Stress and Free Radical Biology Laboratory, University of Calcutta, University College of Science and Technology, 92, APC Road, Kolkata 700 009, West Bengal, India.
Aindrila ChattopadhyayDepartment of Physiology, Vidyasagar College, Kolkata 700 006, India.
Asish R DasDepartment of Chemistry, University of Calcutta, University College of Science and Technology, 92, APC Road, Kolkata 700 009, West Bengal, India.
Debasish BandyopadhyayDepartment of Physiology, Oxidative Stress and Free Radical Biology Laboratory, University of Calcutta, University College of Science and Technology, 92, APC Road, Kolkata 700 009, West Bengal, India.
University of Calcutta · INVidyasagar University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsPreventing mitochondrial dysfunction and enhancing mitochondrial health and biogenesis is a crucial therapeutic approach to ameliorate injury following acute myocardial infarction. Although the antioxidant role of melatonin against ischemia/reperfusion injury has been reported, the exact mechanism of protection, MAIN

methodsRats were pre-treated with melatonin (10 mg/kg body weight (b.w.); intraperitoneally, i.p.) before isoproterenol bitartrate (ISO) administration (25 mg/kg body weight (b.w.) subcutaneously,s.c.) and their effect on rat heart mitochondrial structure and function was studied. Biochemical changes in activity of biomarkers of oxidative stress, antioxidant enzymes as well as Krebs' cycle enzymes were analyzed. Gene expression studies and Isothermal titration calorimetric studies with pure catalase and ISO were also carried out. KEY

findingsMelatonin was shown to reduce ISO induced oxidative stress, by stimulating superoxide dismutase activity and removing the inhibition of Krebs' cycle enzymes. Herein we report for the first time in rat model that melatonin activates the SIRT1-PGC-1α-SIRT3 signaling pathways after ISO administration, which ultimately induces mitochondrial biogenesis. Melatonin exhibited significant protection of mitochondrial architecture and topology along with increased calcium ion permeability and reactive oxygen species (ROS) generation induced by ISO. Isothermal calorimetric studies revealed that melatonin binds to ISO molecules and sequesters them from the reaction thereby limiting their interaction with catalase along with occupying the binding sites of catalase themselves. SIGNIFICANCE: Activation of SIRT1-PGC-1α-SIRT3 pathway by melatonin along with its biophysical properties prevents ISO induced mitochondrial injury in rat heart.

Indexed as

Environmental scienceFood scienceHealth sciencesIsothermal titration calorimetryMelatoninOxidative stressPGC 1αSIRT1SIRT3Veterinary medicine

Identifiers

PMID33088945
PMCPMC7567935
OpenAlexW3093439890

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.