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Mechanisms of Morphogenesis, Degeneration, and Regeneration
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Mechanisms of Morphogenesis, Degeneration, and Regeneration

A Special Issue of Journal of Developmental Biology (ISSN 2221-3759).

Deadline for manuscript submissions: 16 April 2027 | Viewed by 3638

Editors

Dr. Tsutomu Nohno

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Guest Editor
1. Advanced Research Center for Oral and Craniofacial Sciences, Okayama University Dental School, Okayama 700-8525, Japan
2. Department of Cytology and Histology, Okayama University Medical School, Okayama 700-8558, Japan
Interests: musculoskeletal regeneration; limb development; Wnt signaling; microRNA; osteogenesis; myogenesis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Hideyo Ohuchi

E-Mail Website
Guest Editor
Department of Cytology and Histology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan
Interests: histology; developmental biology; regenerative medicine and biology; molecular biology
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Naoyuki Wada

E-Mail Website
Guest Editor
Department of Applied Biological Science, Tokyo University of Science, 2641 Yamazaki, Noda 278-8510, Chiba, Japan
Interests: craniofacial development and regeneration; limb development and regeneration

Special Issue Information

Dear Colleagues,

This Special Issue focuses on the mechanisms of morphogenesis, degeneration, and regeneration, soliciting the latest research findings at the molecular, cellular, and tissue levels that control morphogenesis, tissue/organ degeneration, and regenerative processes in biological development. We welcome studies elucidating how these processes are regulated and interrelated across diverse contexts, including development, physiology, aging, disease, and tissue repair.

This theme covers research including, but not limited to, the following:

  • Molecular and cellular mechanisms of morphogenesis during development;
  • Mechanisms of tissue and organ degeneration and aging;
  • Signaling pathways controlling regeneration and repair processes;
  • Morphogenesis and regeneration studies using model organisms;
  • Applied research for disease and regenerative medicine;
  • Integrating mechanisms to organize tissue and organs through cell–cell interactions.

We seek the latest research findings on molecular, cellular, and tissue-level mechanisms that regulates morphogenesis, tissue and organ degeneration, and regeneration processes in biological development.

Dr. Tsutomu Nohno
Prof. Dr. Hideyo Ohuchi
Prof. Dr. Naoyuki Wada
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 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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Developmental Biology is an international peer-reviewed open access quarterly 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 1800 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

  • morphogenesis
  • tissue degeneration
  • regeneration
  • cell fate determination
  • developmental biology
  • cellular and molecular mechanisms
  • tissue and organ development

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

Published Papers (3 papers)

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Research

16 pages, 3672 KB  
Article
Akhirin Preserves Hemostatic Wound Repair Through Non-Hematopoietic Regulation of the Vascular Injury Microenvironment
by Mohammad Badrul Anam, Mikiko Kudo, Terumasa Umemoto, Keisuke Yamashita, Rie Kawano and Kunimasa Ohta
J. Dev. Biol. 2026, 14(3), 41; https://doi.org/10.3390/jdb14030041 - 7 Sep 2026
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Abstract
Hemostasis and wound healing are highly coordinated processes that involve rapid clot formation followed by controlled remodeling of the injured tissue microenvironment. Prior work on Akhirin (AKH), a secreted extracellular matrix protein containing two von Willebrand factor A domains and an LCCL domain, [...] Read more.
Hemostasis and wound healing are highly coordinated processes that involve rapid clot formation followed by controlled remodeling of the injured tissue microenvironment. Prior work on Akhirin (AKH), a secreted extracellular matrix protein containing two von Willebrand factor A domains and an LCCL domain, has established it as a regulator of the neural stem niche in the developing brain and spinal cord injury microenvironment. However, its role as a non-hematopoietic molecule in the vascular injury response remains unknown. Here, we present evidence that AKH contributes to hemostasis and wound repair outside the neural niche. Our immunohistochemical and biochemical analyses demonstrated AKH around arterial tissues, suggesting a potential role at the blood-vessel interface. AKH-deficient mice exhibited a striking phenotype characterized by prolonged tail bleeding and delayed wound closure, indicating impaired vascular injury repair in vivo. Furthermore, bone marrow transplantation failed to rescue the prolonged bleeding phenotype, supporting a predominant non-hematopoietic contribution. Intriguingly, analysis of classical coagulation revealed an apparent paradox: activated partial thromboplastin time was shortened, whereas prothrombin time was not significantly altered. In contrast, increased expression of tissue plasminogen activator, urokinase-type plasminogen activator, and urokinase-type plasminogen activator receptor in AKH-deficient samples suggested dysregulated local fibrinolytic remodeling. Together, these findings identify AKH as a previously unrecognized extracellular regulator of hemostatic wound repair. Rather than indicating a defect in classical coagulation cascade activation, the findings associate AKH deficiency with impaired hemostatic control and altered expression of plasminogen activator system components, suggesting a role for AKH in the local vascular injury response. Full article
(This article belongs to the Special Issue Mechanisms of Morphogenesis, Degeneration, and Regeneration)
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27 pages, 26954 KB  
Article
CSF1R+ Macrophages and Osteoclasts Are Essential for Limb Bone Development During Embryogenesis
by Felix Ma, Rose Ru Jing Zhou, Matthew Rosin and Jessica M. Rosin
J. Dev. Biol. 2026, 14(3), 31; https://doi.org/10.3390/jdb14030031 - 8 Jul 2026
Viewed by 799
Abstract
Colony-stimulating factor-1 receptor (CSF1R) provides essential signals for macrophage and osteoclast proliferation, differentiation, and survival, but the roles of CSF1R+ macrophages and osteoclasts during limb morphogenesis are understudied. Here, we utilized a pharmacological model by feeding the CSF1R inhibitor PLX5622 to pregnant mice [...] Read more.
Colony-stimulating factor-1 receptor (CSF1R) provides essential signals for macrophage and osteoclast proliferation, differentiation, and survival, but the roles of CSF1R+ macrophages and osteoclasts during limb morphogenesis are understudied. Here, we utilized a pharmacological model by feeding the CSF1R inhibitor PLX5622 to pregnant mice across gestation to examine how CSF1R disruption impacts embryonic limb development. CSF1R-expressing cells were significantly depleted in response to PLX5622 exposure, including a complete loss of embryonic osteoclasts and osteoclastic activity in the developing limb bones. Although the gross morphology of limb nerves, muscles, cartilage, and bone appeared intact between embryonic day 11.5 (E11.5) and E15.5, prenatal PLX5622 exposure resulted in a completely penetrant truncated phenotype for all postnatal day 1 (P1) limb bones analyzed, suggesting that CSF1R+ cells play important roles in mediating limb bone formation during late embryogenesis. Interestingly, strain-specific defects were observed in the heel, where most of the CD1 mice presented with absent talus and underdeveloped calcaneus bones, while the C57BL/6 mice presented with milder developmental disruptions in both bones. Taken together, our data demonstrate that PLX5622 effectively depletes CSF1R-expressing macrophages and osteoclasts in embryonic limbs and suggest an essential role for embryonic CSF1R+ cells in driving limb bone morphogenesis. Full article
(This article belongs to the Special Issue Mechanisms of Morphogenesis, Degeneration, and Regeneration)
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19 pages, 4143 KB  
Article
Expression and Role of Colony Stimulating Factor 1 Receptor During Odontogenesis
by Ashina Nagra, Ling-Yi Chen, Soheil Saeidiborojeni, Jessica M. Rosin and Siddharth R. Vora
J. Dev. Biol. 2026, 14(2), 23; https://doi.org/10.3390/jdb14020023 - 18 May 2026
Viewed by 1097
Abstract
In osteopetrotic mice with homozygous inactivating mutations in the colony stimulating factor 1 (Csf1op/op) or its receptor (Csf1r−/−) gene, teeth fail to erupt due to severe reduction in osteoclastogenesis. Dental abnormalities have been described in the unerupted [...] Read more.
In osteopetrotic mice with homozygous inactivating mutations in the colony stimulating factor 1 (Csf1op/op) or its receptor (Csf1r−/−) gene, teeth fail to erupt due to severe reduction in osteoclastogenesis. Dental abnormalities have been described in the unerupted teeth of these models, but it remains unclear whether these defects arise from direct roles of CSF1R in odontogenesis or indirectly from impaired bone remodeling associated with failed eruption. Here, we examined the spatiotemporal expression of CSF1R during tooth development and inhibited CSF1R pharmacologically in utero using PLX5622 during early stages of tooth morphogenesis. Teeth and surrounding bone were analyzed at embryonic and postnatal stages using histology and high-resolution micro-computed tomography. Embryonic CSF1R inhibition resulted in reproducible abnormalities in incisor and molar morphology that were evident before and after birth and were associated with loss of normal bone remodeling at the tooth–bone interface. In contrast, postnatal CSF1R inhibition did not affect the structure or continuous growth of adult incisors. Together, these findings demonstrate a temporally restricted, indirect role for CSF1R in odontogenesis that is independent of tooth eruption and associated with remodeling of the bony crypts surrounding developing teeth by CSF1R-dependent cells. Full article
(This article belongs to the Special Issue Mechanisms of Morphogenesis, Degeneration, and Regeneration)
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