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Caenorhabditis elegans: A Model Organism for Human Health and Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 December 2024 | Viewed by 1582

Special Issue Editor


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Guest Editor
Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, 4710-057 Braga, Portugal
Interests: C. elegans; disease model; neurodegenerative disorder

Special Issue Information

Dear Colleagues,

The nematode Caenorhabditis elegans offers unique advantages that enable comprehensive research of the cellular and molecular mechanisms underlying human physiology, as well as devastating human pathologies, including neurodevelopmental diseases, age-associated neurodegenerative and neuromuscular disorders, stroke, and cancer.

The tiny worm proved pivotal in uncovering novel cellular mechanisms, including the Nobel prize-winning discoveries of programmed cell death, RNA interference, and the discovery and development of the Green Fluorescent Protein.

The evolutionary conservation between C. elegans and humans led to the establishment of robust C. elegans models of human diseases that closely mimic core disease-related phenotypes. These models allow studies from single-cell resolution to intra- and inter-tissue communication, whole-organism responses to internal and external stimuli, and large-scale genetic and pharmacological screenings. These are designed to elucidate the molecular mechanisms mediating pathogenesis and to identify and validate targets and drugs for emergent therapeutic interventions.

This Special Issue aims to provide an overview of the current research using C. elegans to study all aspects of human health and disease. It also celebrates the 50th anniversary of Sidney Brenner’s seminal paper on the identification of mutations that affect whole-animal behavior, priming a series of groundbreaking scientific discoveries.

Dr. Andreia Teixeira-Castro
Guest Editor

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Keywords

  • human physiology
  • human disease
  • therapy
  • novel C. elegans methods
  • novel C. elegans models
  • disease models

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Published Papers (1 paper)

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Research

10 pages, 2206 KiB  
Article
Isothiocyanate-Rich Moringa Seed Extract Activates SKN-1/Nrf2 Pathway in Caenorhabditis elegans
by Renalison Farias-Pereira, Pierre Camayoc and Ilya Raskin
Int. J. Mol. Sci. 2024, 25(20), 10917; https://doi.org/10.3390/ijms252010917 - 10 Oct 2024
Viewed by 877
Abstract
Moringa oleifera is a tropical tree that has its leaves, fruits, and seeds used as medicine and food. A standardized hydroalcoholic moringa seed extract (MSE) contains up to 40% of an isothiocyanate (MIC-1; moringin), a phytochemical known to have antioxidant and anti-inflammatory properties. [...] Read more.
Moringa oleifera is a tropical tree that has its leaves, fruits, and seeds used as medicine and food. A standardized hydroalcoholic moringa seed extract (MSE) contains up to 40% of an isothiocyanate (MIC-1; moringin), a phytochemical known to have antioxidant and anti-inflammatory properties. Animal studies suggest that MSE may help with diseases, such as edema, colitis, obesity, and diabetes. In vitro studies have shown that MIC-1 activates the Nrf2 pathway, involved in detoxification and antioxidant pathways. To broaden the understanding of the molecular pathways regulated by MSE, we hypothesized that MSE improves the health span in Caenorhabditis elegans by activating the Nrf2 homolog (SKN-1). Our whole RNA-seq data showed that MSE at 0.1 mg/mL (100 µM MIC-1) regulated the expression of a total of 1555 genes, including genes related to C. elegans cuticle, molting cycle, and glutathione metabolism. MSE upregulated several glutathione S transferases (GST), involved in the detoxification of xenobiotics, and other SKN-1 downstream targets. MSE and MIC-1 upregulate skn-1 expression and induce SKN-1 nuclear translocation, suggesting that they activate the SKN-1/Nrf2 pathway. Moreover, the regulation of glutathione metabolism is likely dependent on the SKN-1 pathway, as the gst-4 upregulation by MSE was inhibited in skn-1 knockout mutant. However, MSE decreased survivability and delayed growth rate, while purified MIC-1 increased the lifespan of C. elegans. This study shows that MIC-1 is responsible for SKN-1/Nrf2 activation by MSE; however, components other than MIC-1 within MSE likely cause detrimental effects in C. elegans. Full article
(This article belongs to the Special Issue Caenorhabditis elegans: A Model Organism for Human Health and Disease)
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