Evidence map›Paper›PMID 35689787›Full record

ReviewNeurochemical research2022

Melatonergic Receptors (Mt1/Mt2) as a Potential Additional Target of Novel Drugs for Depression.

Dmytro I Boiko, Anastasiia D Shkodina, Mohammad Mehedi Hasan, Mainak Bardhan, Syeda Kanza Kazmi, Hitesh Chopra, Prerna Bhutra, Atif Amin Baig, Andrii M Skrypnikov

Open access · bronzeAbstract readReview
In one paragraph

Review in Neurochemical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.8field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Endocrine regulation of circadian rhythms.Npj biological timing and sleep · 2025
    Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Melatonin in animal husbandry: functions and applications.Frontiers in veterinary science · 2024
    Review
  18. Review
  19. Article
  20. 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 7 institutions in 5 countries.

Dmytro I BoikoDepartment of Psychiatry, Narcology and Medical Psychology, Poltava State Medical University, Poltava, Ukraine.
Anastasiia D ShkodinaDepartment of Nervous Diseases with Neurosurgery and Medical Genetics, Poltava State Medical University, Poltava, Ukraine.
Mohammad Mehedi HasanDepartment of Biochemistry and Molecular Biology, Faculty of Life Science, Mawlana Bhashani Science and Technology University, Tangail, Bangladesh.
Mainak BardhanDepartment of Neurology, National Institute of Mental Health And Neurosciences (NIMHANS), Bengaluru, India.
Syeda Kanza KazmiDow Medical College, Dow University of Health Sciences, Karachi, Pakistan.
Hitesh ChopraChitkara College of Pharmacy, Chitkara University, Punjab, India. chopraontheride@gmail.com.ORCID http://orcid.org/0000-0001-8867-7603
Prerna BhutraGMERS Medical College and Hospital, Sola, Ahmedabad, Gujarat, India.
Atif Amin BaigFaculty of Medicine, Universiti Sultan Zainal Abidin, Terengganu, Malaysia. atifamin@unisza.edu.my.
Andrii M SkrypnikovDepartment of Psychiatry, Narcology and Medical Psychology, Poltava State Medical University, Poltava, Ukraine.
Poltava State Medical University · UAB.J. Medical College · INChitkara University · INDow University of Health Sciences · PKMawlana Bhashani Science and Technology University · BDNational Institute of Mental Health and Neurosciences · INSultan Zainal Abidin University · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A complex pathogenesis involving several physiological systems is theorized to underline the development of depressive disorders. Depression is accompanied by circadian regulation disruption and interaction with the functioning of both central and peripheral oscillators. Many aspects of melatonin function unite these systems. The use of drugs for circadian rhythm disorders could inspire a potential treatment strategy for depression. Melatonin plays an essential role in the regulation of circadian rhythms. It exerts effect by activating two types of melatonin receptors, type 1A (MT1) and 1B (MT2). These are G-protein-coupled receptors, predominantly located in the central nervous system. MT1/MT2 agonists could be a useful treatment approach according to all three prevalent theories of the pathogenesis of depression involving either monoamines, synaptic remodeling, or immune/inflammatory events. MT1/MT2 receptors can be a potential target for novel antidepressants with impact on concentrations of neurotrophins or neurotransmitters, and reducing levels of pro-inflammatory cytokines. There is an interesting cross-talk mediated via the physical association of melatonin and serotonin receptors into functional heteromers. The antidepressive and neurogenetic effects of MT1/MT2 agonists can also be caused by the inhibition of the acid sphingomyelinase, leading to reduced ceramide, or increasing monoamine oxidase A levels in the hippocampus. Compounds targeting MT1 and MT2 receptors could have potential for new anti-depressants that may improve the quality of therapeutic interventions in treating depression and relieving symptoms. In particular, a combined effect on MT1 and/or MT2 receptors and neurotransmitter systems may be useful, since the normalization of the circadian rhythm through the melatonergic system will probably contribute to improved treatment. In this review, we discuss melatonergic receptors as a potential additional target for novel drugs for depression.

Indexed as

MelatoninAntidepressive AgentsCircadian RhythmDepressionReceptor, Melatonin, MT1Receptor, Melatonin, MT2Antidepressive AgentsMelatoninReceptor, Melatonin, MT1Receptor, Melatonin, MT2Circadian rhythmClock genesDepressionMelatoninNeurogenesisReceptors

Identifiers

PMID35689787
PMCPMC9187850
OpenAlexW4282913161

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.