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Cells
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Breakthroughs in Cell Signaling in Health and Disease
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Breakthroughs in Cell Signaling in Health and Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 4705

Special Issue Editors

Dr. Stephen Yarwood

E-Mail Website
Guest Editor
Institute of Biological Chemistry, Biophysics, and Bioengineering, School of Engineering and Physical Sciences, William Perkin Building, Heriot–Watt University, Edinburgh EH14 4AS, UK
Interests: cell signalling; cyclic AMP; gene expression
Special Issues, Collections and Topics in MDPI journals
Dr. Tuula Kallunki

E-Mail Website1 Website2
Guest Editor
1. Cancer Invasion and Resistance, Danish Cancer Society Research Center, Strandboulevarden 49, DK-2100 Copenhagen, Denmark
2. Department of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen, Denmark
Interests: HER2; breast cancer; invasion; metastasis; drug screening; lysosome; transcription factor; signal transduction; autophagy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cell signaling contributes to homeostasis in humans and is normally involved in endocrine, neuronal and local communication between cells and tissues. However, abnormal cell signaling contributes to many diseases, including chronic inflammation, infection, cancers, neurodegeneration and metabolic disorders. Consequently, research into the mechanisms underlying the control of cell signaling processes in health and disease has accelerated the discovery of disease biomarkers and new drug targets.

As a recognized expert in the field of cell signaling, we are pleased to invite you to contribute original articles, communications and reviews that cover the broad field of “Cell Signaling in Health and Disease”.

Topics will include new mechanisms of signal transduction, the contribution of new mechanisms to functional regulation of cells, tissues, organs and whole organisms and the validation of drug targets and drug development. The Special Issue aims to highlight the recent developments in the signaling field that have a significant impact on our understanding of health and disease.

We look forward to receiving your contributions.

Dr. Stephen Yarwood
Dr. Tuula Kallunki
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 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

  • receptor
  • pathways
  • second messengers
  • human disease

Published Papers (3 papers)

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Research

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15 pages, 2236 KiB  
Article
Uncovering Actions of Type 3 Deiodinase in the Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD)
by Rafael Aguiar Marschner, Ana Cristina Roginski, Rafael Teixeira Ribeiro, Larisse Longo, Mário Reis Álvares-da-Silva and Simone Magagnin Wajner
Cells 2023, 12(7), 1022; https://doi.org/10.3390/cells12071022 - 27 Mar 2023
Cited by 1 | Viewed by 1613
Abstract
Metabolic dysfunction-associated fatty liver disease (MAFLD) has gained worldwide attention as a public health problem. Nonetheless, lack of enough mechanistic knowledge restrains effective treatments. It is known that thyroid hormone triiodothyronine (T3) regulates hepatic lipid metabolism, and mitochondrial function. Liver dysfunction of type [...] Read more.
Metabolic dysfunction-associated fatty liver disease (MAFLD) has gained worldwide attention as a public health problem. Nonetheless, lack of enough mechanistic knowledge restrains effective treatments. It is known that thyroid hormone triiodothyronine (T3) regulates hepatic lipid metabolism, and mitochondrial function. Liver dysfunction of type 3 deiodinase (D3) contributes to MAFLD, but its role is not fully understood. Objective: To evaluate the role of D3 in the progression of MAFLD in an animal model. Methodology: Male/adult Sprague Dawley rats (n = 20) were allocated to a control group (2.93 kcal/g) and high-fat diet group (4.3 kcal/g). Euthanasia took place on the 28th week. D3 activity and expression, Uncoupling Protein 2 (UCP2) and type 1 deiodinase (D1) expression, oxidative stress status, mitochondrial, Krebs cycle and endoplasmic reticulum homeostasis in liver tissue were measured. Results: We observed an increase in D3 activity/expression (p < 0.001) related to increased thiobarbituric acid reactive substances (TBARS) and carbonyls and diminished reduced glutathione (GSH) in the MAFLD group (p < 0.05). There was a D3-dependent decrease in UCP2 expression (p = 0.01), mitochondrial capacity, respiratory activity with increased endoplasmic reticulum stress in the MAFLD group (p < 0.001). Surprisingly, in an environment with lower T3 levels due to high D3 activity, we observed an augmented alpha-ketoglutarate dehydrogenase (KGDH) and glutamate dehydrogenase (GDH) enzymes activity (p < 0.05). Conclusion: Induced D3, triggered by changes in the REDOX state, decreases T3 availability and hepatic mitochondrial capacity. The Krebs cycle enzymes were altered as well as endoplasmic reticulum stress. Taken together, these results shed new light on the role of D3 metabolism in MAFLD. Full article
(This article belongs to the Special Issue Breakthroughs in Cell Signaling in Health and Disease)
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Review

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15 pages, 1893 KiB  
Review
Tissue-Predisposition to Cancer Driver Mutations
by Luriano Peters, Avanthika Venkatachalam and Yinon Ben-Neriah
Cells 2024, 13(2), 106; https://doi.org/10.3390/cells13020106 - 05 Jan 2024
Viewed by 1378
Abstract
Driver mutations are considered the cornerstone of cancer initiation. They are defined as mutations that convey a competitive fitness advantage, and hence, their mutation frequency in premalignant tissue is expected to exceed the basal mutation rate. In old terms, that translates to “the [...] Read more.
Driver mutations are considered the cornerstone of cancer initiation. They are defined as mutations that convey a competitive fitness advantage, and hence, their mutation frequency in premalignant tissue is expected to exceed the basal mutation rate. In old terms, that translates to “the survival of the fittest” and implies that a selective process underlies the frequency of cancer driver mutations. In that sense, each tissue is its own niche that creates a molecular selective pressure that may favor the propagation of a mutation or not. At the heart of this stands one of the biggest riddles in cancer biology: the tissue-predisposition to cancer driver mutations. The frequency of cancer driver mutations among tissues is non-uniform: for instance, mutations in APC are particularly frequent in colorectal cancer, and 99% of chronic myeloid leukemia patients harbor the driver BCR-ABL1 fusion mutation, which is rarely found in solid tumors. Here, we provide a mechanistic framework that aims to explain how tissue-specific features, ranging from epigenetic underpinnings to the expression of viral transposable elements, establish a molecular basis for selecting cancer driver mutations in a tissue-specific manner. Full article
(This article belongs to the Special Issue Breakthroughs in Cell Signaling in Health and Disease)
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14 pages, 1356 KiB  
Review
Tumor Angiocrine Signaling: Novel Targeting Opportunity in Cancer
by Victor Oginga Oria and Janine Terra Erler
Cells 2023, 12(20), 2510; https://doi.org/10.3390/cells12202510 - 23 Oct 2023
Viewed by 1088
Abstract
The vascular endothelium supplies nutrients and oxygen to different body organs and supports the progression of diseases such as cancer through angiogenesis. Pathological angiogenesis remains a challenge as most patients develop resistance to the approved anti-angiogenic therapies. Therefore, a better understanding of endothelium [...] Read more.
The vascular endothelium supplies nutrients and oxygen to different body organs and supports the progression of diseases such as cancer through angiogenesis. Pathological angiogenesis remains a challenge as most patients develop resistance to the approved anti-angiogenic therapies. Therefore, a better understanding of endothelium signaling will support the development of more effective treatments. Over the past two decades, the emerging consensus suggests that the role of endothelial cells in tumor development has gone beyond angiogenesis. Instead, endothelial cells are now considered active participants in the tumor microenvironment, secreting angiocrine factors such as cytokines, growth factors, and chemokines, which instruct their proximate microenvironments. The function of angiocrine signaling is being uncovered in different fields, such as tissue homeostasis, early development, organogenesis, organ regeneration post-injury, and tumorigenesis. In this review, we elucidate the intricate role of angiocrine signaling in cancer progression, including distant metastasis, tumor dormancy, pre-metastatic niche formation, immune evasion, and therapy resistance. Full article
(This article belongs to the Special Issue Breakthroughs in Cell Signaling in Health and Disease)
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