Melatonin Signaling: Therapeutic Implications and Molecular Mechanisms

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: 15 May 2026 | Viewed by 81

Special Issue Editors


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Guest Editor
1. Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
2. Graduate Institute of Aerospace and Undersea Medicine, National Defense Medical Center, Taipei, Taiwan
Interests: melatonin receptor; membranous nephropathy; non-coding RNA
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Division of Nephrology, Department of Medicine, Tri-Service General Hospital, Taipei, Taiwan
Interests: melatonin; nephritic syndrome; nephrotic syndrome

Special Issue Information

Dear Colleagues,

Melatonin is a chronobiotic hormone; it follows a process that is tightly upregulated primarily in the pineal gland and the suprachiasmatic nucleus via the enzymes AANAT and HIOMT. Melatonin orchestrates a broad spectrum of physiological functions in a melatonin receptor-dependent or -independent manner. These functions include regulating circadian rhythms, scavenging free radicals, acting as an anti-inflammatory agent, modulating mitochondrial homeostasis, functioning as an antioxidant, and enhancing nitric oxide bioavailability. Melatonin regulates gene expression in a receptor-dependent manner through physiological pathways that include the MAPK pathway, the cGMP/PKC pathway, the cAMP/PKA pathway, and the PI3K/AKT and PLCb pathways. Exogenous melatonin and synthetic agonists are increasingly recognized for their therapeutic potential beyond sleep, extending to various disease conditions linked to circadian disruption or melatonin deficiency.

Single-nucleotide polymorphisms (SNPs) close to melatonin receptor genes, as well as downregulated melatonin receptor levels, have been observed in diseases or specific physiological states, but there is a lack of significant experiments to demonstrate the functions of these SNPs or decreased levels. Moreover, a knowledge gap persists regarding the molecular regulation of endogenous melatonin production and melatonin receptor expression in peripheral tissues. The development of novel drugs aimed at enhancing melatonin expression or melatonin receptor levels represents a promising new direction for melatonin signaling therapy. While the evolutionary conservation of melatonin signaling across diverse species is remarkable, more research is needed to fully leverage these cross-species insights. By exploring both the conserved and divergent aspects of melatonin's actions across species, this collection will aim to identify novel therapeutic targets and strategies centered around melatonin signaling for various human conditions.

This collection invites original research articles, reviews, mini reviews, and perspectives. The research topic defines its scope by listing specific themes for contributors, including, but not limited to, the following:

  • Therapeutic insights and molecular mechanisms linking melatonin signaling with various diseases;
  • Optimizing melatonin or melatonin pathway agonist treatment for disease intervention;
  • Melatonin receptor structure and signaling;
  • Melatonin synthesis and melatonin receptor function in diverse organisms;
  • Molecular characterization and pharmacological profiling of melatonin receptors and melatonin-synthesizing enzymes.

We encourage submissions that employ multidisciplinary approaches to advance our understanding of melatonin signaling.

Dr. Yen-Sung Huang
Dr. Chia-Chao Wu
Guest Editors

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • melatonin
  • AANAT
  • HIOMT
  • MTNR1A
  • MTNR1B
  • circadian rhythms

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Published Papers

This special issue is now open for submission.
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