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Biomedicines
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Mechanobiology and Extracellular Vesicle-Based Strategies for Osteochondral Regeneration
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Mechanobiology and Extracellular Vesicle-Based Strategies for Osteochondral Regeneration

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Biomedical Engineering and Materials".

Deadline for manuscript submissions: 30 December 2026 | Viewed by 3679

Editor

Dr. Zhen Yang

E-Mail Website
Guest Editor
Arthritis Clinical and Research Center, Peking University People’s Hospital, Beijing 100044, China
Interests: cartilage and meniscus tissue engineering

Special Issue Information

Dear Colleagues,

This Special Issue will focus on emerging strategies for musculoskeletal regeneration by integrating biomechanics, stem cell biology, extracellular vesicles, and advanced tissue engineering approaches. We welcome original research articles and reviews that explore the mechanobiological regulation of stem cell fate, the role of extracellular vesicles in osteoarthritis pathogenesis and therapy, and the development of osteochondral organoids or biomaterial-based systems for translational applications. The goal is to provide a multidisciplinary platform linking fundamental mechanisms with innovative therapeutic strategies for osteoarthritis and related joint diseases.

Dr. Zhen Yang
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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines 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

  • biomechanics
  • stem cells
  • osteoarthritis
  • tissue engineering
  • extracellular vesicles

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Published Papers (3 papers)

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Research

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31 pages, 40972 KB  
Article
BDNF-Hyaluronic Acid Hydrogel Promotes Neuronal Differentiation of Neural Stem Cells in Aβ-Induced Injury and 5×FAD Mice
by Kangzhen Chen, Hehang Shi, Yuanyuan Bai, Shengbo Shi, Baoqing Gao, Hongmei Duan, Peng Hao, Wen Zhao, Yudan Gao, Zhaoyang Yang and Xiaoguang Li
Biomedicines 2026, 14(6), 1316; https://doi.org/10.3390/biomedicines14061316 - 10 Jun 2026
Viewed by 460
Abstract
Objectives: Alzheimer’s disease (AD) is associated with impaired adult hippocampal neurogenesis (AHN). This study aimed to establish an in vitro model of Aβ1–42 oligomer-damaged neural stem cells (NSCs) and to employ the 5×FAD mouse model of AD in vivo, and to [...] Read more.
Objectives: Alzheimer’s disease (AD) is associated with impaired adult hippocampal neurogenesis (AHN). This study aimed to establish an in vitro model of Aβ1–42 oligomer-damaged neural stem cells (NSCs) and to employ the 5×FAD mouse model of AD in vivo, and to evaluate the therapeutic effects of brain-derived neurotrophic factor-loaded hyaluronic acid hydrogel (BDNF-HA gel) on AHN. Methods: In vitro, BDNF-HA gel was co-cultured with Aβ1–42 oligomer-impaired NSC spheres and evaluate NSC proliferation, migration, and differentiation. In vivo, BDNF-HA gel was infused intracerebroventricularly into 5×FAD mice. Using BrdU labeling, immunofluorescence, anterograde transsynaptic viral tracing, and behavioral tests, we assessed the effects of BDNF-HA gel on adult neurogenesis, newborn neuron integration into memory circuits, and cognitive function. Results: In vitro, BDNF-HA gel attenuated Aβ1–42-induced NSC apoptosis, restored proliferation and migration, promoted differentiation into neuroblasts, newborn neurons, and oligodendrocytes, and alleviated mitochondrial depolarization and loss of mitochondrial mass. In vivo, despite the absence of significant Aβ plaques reduction in 5×FAD mice, BDNF-HA gel markedly enhanced NSC proliferation and neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ). Behavioral tests further revealed significant improvements in object recognition, spatial working memory, and spatial reference memory. Conclusions: BDNF-HA gel can effectively counteract the toxic microenvironment induced by Aβ oligomers, promoting NSC proliferation, migration, and differentiation into neurons. Without altering the Aβ burden, it significantly enhances adult neurogenesis and rescues cognitive deficits in AD mice. Full article
(This article belongs to the Special Issue Mechanobiology and Extracellular Vesicle-Based Strategies for Osteochondral Regeneration)
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16 pages, 8121 KB  
Article
All-Trans Retinoic Acid Impacts Early Palatal Shelves Development via the Wnt and TGF-β Signaling Pathways
by Yaping Ma, Binqing Wang, Shikang Gao and Tao Song
Biomedicines 2025, 13(11), 2836; https://doi.org/10.3390/biomedicines13112836 - 20 Nov 2025
Cited by 1 | Viewed by 1077
Abstract
Background/Objectives: All-trans retinoic acid (atRA), a potent derivative of vitamin A, is recognized as a significant teratogen for inducing cleft palate in both humans and mice. The molecular mechanisms underlying it remain intricate and incompletely elucidated. The advent of single-cell sequencing technology offers [...] Read more.
Background/Objectives: All-trans retinoic acid (atRA), a potent derivative of vitamin A, is recognized as a significant teratogen for inducing cleft palate in both humans and mice. The molecular mechanisms underlying it remain intricate and incompletely elucidated. The advent of single-cell sequencing technology offers novel methodologies to investigate the mechanisms by which atRA induces cleft palate. Methods: In this study, we use C57BL/6 mice to conduct cleft palate models, comprising a control group and an atRA-exposed group. Palatal shelves were collected at embryonic day 12.5 (E12.5) for 10x single-cell sequencing analysis to discern and compare the cellular and molecular disparities between the two groups. Validation of the findings was performed using Quantitative real-time polymerase chain reaction and Western blot techniques. Results: The findings indicate that at E12.5, atRA predominantly affects the mesenchymal and epithelial cells of the palatal shelves, inhibiting cellular proliferation and migration. The primary mechanism of atRA’s effect involves modulation of the Wnt and TGF-β signaling pathways. Furthermore, the Ppp1r14b gene was identified as a critical mediator in atRA’s interaction with these pathways. Conclusions: This study provides a more comprehensive understanding of the mechanisms underlying atRA-induced cleft palate formation. It highlights the significance of the Wnt and TGF-β pathways, as well as the Ppp1r14b gene during this procedure. Full article
(This article belongs to the Special Issue Mechanobiology and Extracellular Vesicle-Based Strategies for Osteochondral Regeneration)
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Review

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17 pages, 1928 KB  
Review
Beyond ER Stress: The Pleiotropic Roles of XBP1 in Development and Regeneration
by Delan Huang, Fan Gu, Jingzhi Ma and Zhi Chen
Biomedicines 2025, 13(11), 2663; https://doi.org/10.3390/biomedicines13112663 - 30 Oct 2025
Viewed by 1604
Abstract
This review synthesizes current knowledge on the roles of X-box binding protein 1 (XBP1) in development and regenerative medicine. XBP1 is defined as a key transcription factor that regulates biological processes from embryogenesis to adult tissue homeostasis via both endoplasmic reticulum(ER) stress-dependent and [...] Read more.
This review synthesizes current knowledge on the roles of X-box binding protein 1 (XBP1) in development and regenerative medicine. XBP1 is defined as a key transcription factor that regulates biological processes from embryogenesis to adult tissue homeostasis via both endoplasmic reticulum(ER) stress-dependent and independent mechanisms. Evidence for its regulatory role in cell fate determination and tissue maintenance across multiple systems is presented. The therapeutic potential of targeting XBP1 is explored, particularly for the regeneration of skeletal muscle, skin, and bone. Critical future research priorities are outlined, such as deciphering the precise functions of the Inositol requiring enzyme 1 (IRE1α)/XBP1 signaling axis and evaluating the long-term safety of its modulation. XBP1 is thus confirmed as a prime target for advancing developmental biology and pioneering new regenerative therapies. Full article
(This article belongs to the Special Issue Mechanobiology and Extracellular Vesicle-Based Strategies for Osteochondral Regeneration)
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