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Life
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Cell Regulation and Function
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Cell Regulation and Function

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Cell Biology and Tissue Engineering".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 1009

Special Issue Editor

Dr. Tada-aki Kudo

E-Mail Website
Guest Editor
Division of Oral Physiology, Tohoku University Graduate School of Dentistry, Sendai 980-8575, Japan
Interests: physical stimulations inducing cell differentiation; cell signaling; neural regeneration; bone remodeling; taste sensitivity and preference
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cells are the fundamental units of life, executing a wide range of biological functions through tightly regulated molecular and structural mechanisms. From signal transduction and gene expression to organelle dynamics and metabolic coordination, cellular regulation ensures both the maintenance of homeostasis and responsiveness to environmental cues. These regulatory processes are essential not only for normal development and tissue function but also for the progression of various diseases, including cancer, neurodegeneration, and immune disorders.

Recent advances in imaging, omics technologies, and computational modeling have provided unprecedented insights into the spatial and temporal orchestration of cellular functions. Furthermore, the integration of systems biology approaches has uncovered new layers of complexity in cell behavior and regulation.

This Special Issue, entitled “Cell Regulation and Function”, welcomes contributions from all areas of in vivo and in vitro research that explore novel physiological and pathological mechanisms of cellular regulation.

Dr. Tada-aki Kudo
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 250 words) can be sent to the Editorial Office for assessment.

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. Life is an international peer-reviewed open access monthly 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 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

  • cellular regulation
  • signal transduction
  • cell differentiation and apoptosis
  • systems biology and omicsdisease mechanisms

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

23 pages, 32585 KB  
Article
Mechanobiological and Molecular Alterations in the Aging Dentin–Pulp Complex
by Neshka Manchorova-Veleva, Mina Pencheva, David Baruh, Veselina Todorova, Lyubomir Vangelov, Evgeni Ivanov and Margarita Guenova
Life 2026, 16(5), 844; https://doi.org/10.3390/life16050844 (registering DOI) - 20 May 2026
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Abstract
The dental pulp–dentin complex is a dynamic tissue system whose structure and biological functions evolve over time under physiological, molecular, and environmental influences. This study aimed to characterize age-related alterations in apoptotic, inflammatory, and autophagy-associated signaling pathways, alongside nanoscale mechanical changes, and to [...] Read more.
The dental pulp–dentin complex is a dynamic tissue system whose structure and biological functions evolve over time under physiological, molecular, and environmental influences. This study aimed to characterize age-related alterations in apoptotic, inflammatory, and autophagy-associated signaling pathways, alongside nanoscale mechanical changes, and to evaluate their potential impact on pulp tissue homeostasis and cellular adaptive capacity. Materials and Methods: Human teeth (n = 90) were divided into three age groups: young (≤17 years), mature (18–50 years), and old (>51 years). Immunohistochemistry was performed to assess the expression of CD34, BID, Caspase-8, NFκB, STAT3, JAK1, COX-2, LAMP2, and MAP LC3II. Nanoindentation and atomic force microscopy (AFM) were used to measure dentin hardness and modulus of elasticity. Results: BID expression increased with age, whereas Caspase-8 showed a relative decrease (p < 0.05). Anterior teeth exhibited higher marker positivity than molars for BID (p = 0.029), Caspase-8 (p = 0.004), STAT3 (p = 0.001), and JAK1 (p = 0.026). Mechanical analysis revealed the lowest modulus of elasticity in young root dentin and the highest in old coronal dentin, reflecting progressive age-dependent structural changes. Conclusions: Aging of the dentin–pulp complex involves coordinated modulation of apoptotic, autophagic, and inflammatory pathways, closely linked to altered mechanical properties. This interplay likely influences pulp vitality and adaptive cellular responses, highlighting potential targets for age-adapted dental therapeutic strategies. Full article
(This article belongs to the Special Issue Cell Regulation and Function)
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22 pages, 1789 KB  
Article
Effects of the Uncoupling Protein 1 (UCP1) A-3826G Polymorphism on Taste Preferences in Healthy Young Japanese Adults
by Toshishige Kokubun, Tada-aki Kudo, Kanako Tominami, Hirotaka Ishigaki, Ayumu Matsushita, Satoshi Izumi, Takakuni Tanaka, Kotoku Kawaguchi, Yohei Hayashi, Hajime Sato, Naoki Shoji, Keiko Gengyo-Ando, Kazunori Adachi, Junichi Nakai and Guang Hong
Life 2026, 16(3), 499; https://doi.org/10.3390/life16030499 - 18 Mar 2026
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Abstract
Background: The UCP1 A-3826G polymorphism, located in the gene’s regulatory region, is associated with obesity and altered fat metabolism. Because UCP1 plays a central role in thermogenesis, variation in its expression may influence metabolic efficiency and dietary fat preference. Methods: We examined associations [...] Read more.
Background: The UCP1 A-3826G polymorphism, located in the gene’s regulatory region, is associated with obesity and altered fat metabolism. Because UCP1 plays a central role in thermogenesis, variation in its expression may influence metabolic efficiency and dietary fat preference. Methods: We examined associations between the A-3826G polymorphism and food preferences in healthy young Japanese adults (50 males, 48 females). Preferences for high-fat and basic-taste foods were assessed using a self-administered questionnaire, with sweet foods classified as low- or high-fat. Genotypes (AA, AG, GG) were analyzed using a two-way mixed-design ANOVA to evaluate genotype × fat level interactions. Results: Preference scores for basic tastes did not differ significantly among genotypes in either sex (except for sour taste in males). In males, no significant genotype × fat level interaction was observed, although AA carriers preferred high-fat to low-fat sweet foods (p < 0.05). In females, a significant genotype × fat level interaction was detected (p < 0.01), with AG carriers showing lower preference for high-fat sweet foods. Conclusions: These findings indicate that the UCP1 A-3826G polymorphism may modulate preference for high-fat sweet foods in a sex-dependent manner, suggesting a link between thermogenic genetic variation and dietary fat preference relevant to obesity prevention. Full article
(This article belongs to the Special Issue Cell Regulation and Function)
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