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Cells
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Translational Aspects of Cell Signaling
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Translational Aspects of Cell Signaling

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 30 October 2026 | Viewed by 4543

Special Issue Editor

Prof. Dr. Marc D. Basson

E-Mail Website
Guest Editor
College of Medicine, Northeast Ohio Medical University, Rootstown, OH 44272, USA
Interests: mucosal healing; cancer biology; surgery
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Our understanding of the intricacies of cell signaling has increased exponentially over the past decades, and we are increasingly coming to understand the complexities and interactions between different signals and how they are regulated, including proteins, various species of RNA, and other moieties. While the signaling itself is fascinating, it also offers the opportunity to identify new targets by which we can intervene and affect change in the physiology or pathophysiology of the organism. Whether developing new drugs to treat disease or identifying predictive markers of subsequent outcomes, or even intervening to promote health, such signaling targets represent the future of medicine. This Special Issue offers the opportunity to glimpse that future.

Prof. Dr. Marc D. Basson
Guest Editor

Manuscript Submission Information

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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

  • cell signaling
  • drug development
  • prognostic markers
  • bioinformatics
  • translational research

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Published Papers (4 papers)

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Research

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15 pages, 18845 KB  
Article
FGF2 Deficiency Modulates Early Microglial Responses Without Affecting Photoreceptor Survival in a Retinitis Pigmentosa Mouse Model
by Felia C. Haffelder, Nundehui Díaz-Lezama, Zeynep Okutan, Claudia Grothe and Susanne F. Koch
Cells 2026, 15(7), 643; https://doi.org/10.3390/cells15070643 - 2 Apr 2026
Viewed by 556
Abstract
Fibroblast growth factor 2 (FGF2) is expressed in retinal Müller glia cells, and its expression increases in response to photoreceptor degeneration. To investigate the physiological relevance of FGF2, we analyzed retinal morphology and cellular responses in Fgf2-deficient (Fgf2−/−) mice. [...] Read more.
Fibroblast growth factor 2 (FGF2) is expressed in retinal Müller glia cells, and its expression increases in response to photoreceptor degeneration. To investigate the physiological relevance of FGF2, we analyzed retinal morphology and cellular responses in Fgf2-deficient (Fgf2−/−) mice. Loss of FGF2 did not affect photoreceptor survival, retinal vasculature, or retinal pigment epithelium (RPE) integrity. To further understand its role in retinal degeneration, Fgf2−/− mice were crossed with Pde6bSTOP/STOP mice, a model of retinitis pigmentosa (RP). We then analyzed outer nuclear layer thickness, cone number, rod outer segments length, RPE morphology, and microglia number in Fgf2−/− Pde6bSTOP/STOP and Pde6bSTOP/STOP mice. Although FGF2 was upregulated in degenerating photoreceptor cells in the Pde6bSTOP/STOP retina, its absence did not accelerate photoreceptor loss in Fgf2−/− Pde6bSTOP/STOP mice. Interestingly, microglia numbers were significantly changed at early disease stages in Fgf2−/− Pde6bSTOP/STOP retinas compared with Pde6bSTOP/STOP controls, suggesting that FGF2 modulates inflammatory signaling. Together, these results show that loss of FGF2 does not alter photoreceptor degeneration kinetics or retinal morphology, but may contribute to the regulation of early microglial accumulation during degeneration. Full article
(This article belongs to the Special Issue Translational Aspects of Cell Signaling)
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15 pages, 3092 KB  
Article
Short-Chain Fatty Acids and Palmitate Induce Distinct Metabolic and Phenotypic Signatures in Normal and Ischemic Skeletal Muscle Microvascular Endothelial Cells
by Andrew Guilfoyle-Speese, Kripa Patel, Aishwarya H. Ghanwat, David Stepp and Vijay Ganta
Cells 2026, 15(6), 493; https://doi.org/10.3390/cells15060493 - 10 Mar 2026
Viewed by 608
Abstract
Background: Palmitate, a long-chain fatty acid, is well known to be a significant risk factor for cardiovascular diseases. In our current study, we wanted to determine whether palmitate treatment further aggravates ischemic endothelial cell (EC) injury and can serve as an in [...] Read more.
Background: Palmitate, a long-chain fatty acid, is well known to be a significant risk factor for cardiovascular diseases. In our current study, we wanted to determine whether palmitate treatment further aggravates ischemic endothelial cell (EC) injury and can serve as an in vitro model that emulates diabetic peripheral artery disease (diabetic-PAD). Short-chain fatty acid (SCFA) treatment was used as an additional comparator for palmitate-induced vascular dysfunction in normal or ischemic ECs in vitro. Methods: Hypoxia serum starvation (HSS) was used as an in vitro model for PAD. Cell survival or proliferation was determined by the CCK8 kit. EC angiogenic capacity was determined by in vitro tube formation assays on growth factor-reduced Matrigel. EC barrier integrity was determined by trans-endothelial electrical resistance measurements by EVOM3. EC metabolic phenotyping was performed by Seahorse glycolysis, mitochondrial respiration, and fatty acid oxidation metabolic assays. Results: Palmitate dramatically decreased the survival of normal and ischemic ECs, whereas SCFAs did not have a significant effect on ischemic EC survival. In vitro angiogenic assays showed that palmitate significantly decreased the angiogenic capacity of ischemic ECs, whereas SCFAs significantly induced their angiogenic capacity. While palmitate significantly decreased normal and ischemic EC barrier integrity, SCFAs improved normal and ischemic EC barrier integrity. Metabolic assays showed that palmitate significantly decreased normal EC mitochondrial respiration but not glycolysis. However, palmitate significantly decreased overall metabolic health, including mitochondrial respiration and glycolysis in ischemic ECs. On the contrary, SCFAs increased both mitochondrial respiration and glycolysis in normal ECs. In ischemic ECs, SCFAs induced mitochondrial respiration with a concomitant decrease in glycolysis. Fatty acid oxidation analysis showed that, unlike palmitate, which depends on carnitine palmitoyl transferases (CPTs) for β-oxidation in both normal and HSS ECs, SCFAs depend partly on CPTs to undergo β-oxidation in HSS ECs but not in normal ECs. Conclusions: While palmitate inhibits ischemic EC angiogenic capacity by decreasing overall metabolic health, SCFAs induce glycolysis–mitochondria OxPhos coupling to induce ischemic EC angiogenic capacity. Full article
(This article belongs to the Special Issue Translational Aspects of Cell Signaling)
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24 pages, 7533 KB  
Article
FAK-Activated Mucosal Healing Promotes Resistance to Reinjury
by Sema Oncel, Guiming Liu, Louis Kwantwi, Emilie E. Vomhof-DeKrey, Ricardo Gallardo-Macias, Vadim J. Gurvich and Marc D. Basson
Cells 2026, 15(1), 16; https://doi.org/10.3390/cells15010016 - 22 Dec 2025
Cited by 1 | Viewed by 1047
Abstract
Background: Gastrointestinal (GI) mucosal injury is a frequent complication of long-term nonsteroidal anti-inflammatory drug (NSAID) use. Effective mucosal healing requires coordinated epithelial migration, proliferation, and angiogenesis, which may be influenced by focal adhesion kinase (FAK). This study aimed to determine whether our newly [...] Read more.
Background: Gastrointestinal (GI) mucosal injury is a frequent complication of long-term nonsteroidal anti-inflammatory drug (NSAID) use. Effective mucosal healing requires coordinated epithelial migration, proliferation, and angiogenesis, which may be influenced by focal adhesion kinase (FAK). This study aimed to determine whether our newly developed FAK activators promote intestinal mucosal healing by enhancing angiogenesis and whether FAK activation increases resistance to reinjury. Methods: Ischemic jejunal ulcers were induced in C57BL/6 mice. After 24 h, mice received intraperitoneal injections of the FAK activator ZINC40099027 (ZN27, 900 µg/kg every 6 h) or vehicle for 2, 4, or 14 days. Ulcer areas were quantified, and liver and kidney function were assessed. Ulcer and adjacent tissues were analyzed by immunofluorescence staining for angiogenesis and proliferation markers. In vitro, human umbilical vein endothelial cells (HUVECs) were treated with ZN27 to evaluate proliferation, migration, angiogenesis, and intracellular signaling. In a reinjury model, male C57BL/6J mice received continuous infusion of the FAK activator M64HCl (25 mg/kg/day) or vehicle for 7 days, with a single subcutaneous injection of indomethacin (10 mg/kg) on day 1 to induce GI injury. Fourteen days after the first dose of indomethacin, the mice received a second indomethacin challenge, and one day later, total ulcer areas in the pyloric opening and small intestine were quantified. Results: Ulcer areas were significantly smaller in ZN27-treated mice compared with vehicle-treated controls at 3 and 5 days, accompanied by increased expression of angiogenesis and proliferation markers. In vitro, ZN27 enhanced HUVEC migration via FAK activation in an ERK1/2-dependent manner and increased the number of angiogenic sprouts. In the reinjury model, treatment with M64HCl during the initial indomethacin-induced injury resulted in significantly smaller ulcer areas in both the pyloric opening and small intestine after the second indomethacin challenge compared with controls. Conclusions: FAK activation accelerates ischemic ulcer healing, in part by enhancing angiogenesis. Moreover, FAK activation during an initial injury reduces susceptibility to recurrent NSAID-induced intestinal injury, perhaps because it promotes initial higher-quality ulcer repair. Full article
(This article belongs to the Special Issue Translational Aspects of Cell Signaling)
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Review

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30 pages, 3986 KB  
Review
Mathematical Modeling of Cell Death and Survival: Toward an Integrated Computational Framework for Multi-Decision Regulatory Dynamics
by Elena Kutumova, Ilya Akberdin, Inna Lavrik and Fedor Kolpakov
Cells 2025, 14(22), 1792; https://doi.org/10.3390/cells14221792 - 14 Nov 2025
Cited by 2 | Viewed by 1859
Abstract
Mathematical modeling is essential for understanding the complex regulatory pathways governing cell death and survival, including apoptosis, necroptosis, pyroptosis, ferroptosis, autophagy, and immunogenic cell death (ICD)—a functional category comprising diverse morphological types capable of activating immune responses. The growing number of models describing [...] Read more.
Mathematical modeling is essential for understanding the complex regulatory pathways governing cell death and survival, including apoptosis, necroptosis, pyroptosis, ferroptosis, autophagy, and immunogenic cell death (ICD)—a functional category comprising diverse morphological types capable of activating immune responses. The growing number of models describing individual signaling pathways poses the challenge of integrating them into a cohesive framework. This review aims to identify common components across existing ordinary differential equation models that could serve as key nodes to merge distinct signaling modalities. Proposed models highlight Bcl-2, Bax, Ca2, and p53 as shared regulators linking autophagy and apoptosis. Necroptosis and apoptosis are interconnected via TNF signaling network and modulated by caspase-8, c-FLIP, and NFκB, with RIPK1 acting as a critical hub directing pathway choice. Pyroptosis and apoptosis are co-regulated by NFκB, tBid, and caspases, while ferroptosis is modeled exclusively as an independent process, separate from other forms of cell death. Furthermore, existing models indicate that ICD intersects with necroptosis during oncolytic virotherapy, with pyroptosis in SARS-CoV-2 infection, and with apoptosis in the context of chemotherapy. Although several models address crosstalk between pairs of cell fate decisions, creating comprehensive frameworks that encompass three or more death modes remains an open challenge. Full article
(This article belongs to the Special Issue Translational Aspects of Cell Signaling)
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