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Cells
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Cellular Pathology: Emerging Discoveries and Perspectives in the USA
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Cellular Pathology: Emerging Discoveries and Perspectives in the USA

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

Deadline for manuscript submissions: 28 February 2026 | Viewed by 1086

Special Issue Editor

Prof. Dr. Mohammed S. Razzaque

E-Mail Website
Guest Editor
Department of Medical Education, School of Medicine, University of Texas (UTRGV), 1204 W Schunior Street, Edinburg, TX 78541, USA
Interests: pathomechanisms behind renal injury; nutrition and aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are excited to launch this Special Issue, "Cellular Pathology: Emerging Discoveries and Perspectives in the USA". In the rapidly evolving scientific landscape, cell pathology remains at the forefront of exploration and discovery. This Special Issue will serve as a platform to showcase advancements and insights emerging from the vibrant scientific community in the USA. We invite research papers that will consolidate our understanding in this area, focusing primarily on the mechanisms underlying disease processes and the characterization of cellular pathways relevant to pathogenicity. Recent advancements in image-based digital pathology and molecular pathology have led to discoveries that have significantly advanced diagnostic capabilities, therapeutic strategies, and our understanding of cellular pathology in general. This Special Issue will include research articles and comprehensive reviews on various aspects of cardiovascular health, metabolic health, cognitive health, genetic diseases, hepatorenal diseases, respiratory diseases, and tumorigenesis

We thank you in advance for your participation in this exciting journey of discovery, and we look forward to sharing your remarkable contributions in this Special Issue, "Cellular Pathology: Emerging Discoveries and Perspectives in the USA".

Prof. Dr. Mohammed S. Razzaque
Guest Editor

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

  • cellular pathology
  • diseases
  • mechanisms

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Published Papers (1 paper)

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Research

24 pages, 8054 KiB  
Article
INHIBITION OF THE PROSTAGLANDIN-DEGRADING ENZYME 15-PGDH AMELIORATES MASH-ASSOCIATED APOPTOSIS AND FIBROSIS IN MICE
by Utibe-Abasi S. Udoh, Mathew Steven Schade, Jacqueline A. Sanabria, Pradeep Kumar Rajan, Rodrigo Aguilar, Micheal Andryka, Alexei Gorka, Sandrine V. Pierre and Juan Sanabria
Cells 2025, 14(13), 987; https://doi.org/10.3390/cells14130987 - 27 Jun 2025
Viewed by 641
Abstract
Background. Metabolic dysfunction-associated steatotic liver disease (MASLD) affects more than 30% of the world population. Progression to its inflammatory state, MASH, is associated with increasing liver fibrosis, leading to end-stage liver disease (ESLD) and hepatocellular carcinoma (HCC). SW033291, an inhibitor of 15-PGDH [...] Read more.
Background. Metabolic dysfunction-associated steatotic liver disease (MASLD) affects more than 30% of the world population. Progression to its inflammatory state, MASH, is associated with increasing liver fibrosis, leading to end-stage liver disease (ESLD) and hepatocellular carcinoma (HCC). SW033291, an inhibitor of 15-PGDH (the PGE2 degradation enzyme), has been shown to increase in vivo regeneration of liver parenchyma, ameliorating oxidative stress and inflammation. We hypothesized that SW033291 abrogates MASH progression by inducing a paucity of the initial apoptotic switch and restoring physiological collagen’s microenvironment. Methods. The expression levels of the cell metabolic proteins FOXO1, mTOR, and SIRT7 were determined in a diet-induced MASH-mouse model at 16, 20, and 24 weeks. Non-targeted metabolomics in mouse plasma were measured by LC-MS/MS. Liver morphology and apoptotic activity were quantified by the NAS score and TUNEL assay, respectively. Statistical analyses between groups (NMC, HFD, and SW033291) were determined by ANOVA, t-test/Tukey’s post hoc test using GraphPad Prism. Metabolomics data were analyzed using R-lab. Results. The treated group showed significant decreases in total body fat, cellular oxidative stress, and inflammation and an increase in total lean mass with improved insulin resistance and favorable modulation of metabolic protein expressions (p < 0.05). SW033291 significantly decreased GS:SG, citric acid, and corticosterone, NAS scores (9.4 ± 0.2 vs. 6.2 ± 0.1, p < 0.05), liver fibrosis scores (1.3 ± 0.5 vs. 0.25 ± 0.1, p < 0.05), and apoptotic activity (43.9 ± 4.6 vs. 0.38 ± 0.1%, p < 0.05) compared with controls at 24W. Conclusions. The inhibition of 15-PGDH appears to normalize the metabolic and morphological disturbances during MASH progression with a paucity of the initial apoptotic switch, restoring normal collagen architecture. SW033291 warrants further investigation for its translation. Full article
(This article belongs to the Special Issue Cellular Pathology: Emerging Discoveries and Perspectives in the USA)
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