Topic Editors

The BioRobotics Institute, Scuola Superiore Sant’Anna, Piazza Martiri della Libertà 33, 56127 Pisa, Italy
Department of Excellence in Robotics and AI, The BioRobotics Institute, Scuola Superiore Sant’Anna, 56127 Pisa, Italy

Biofabrication Technologies for Tissue Repair and Regeneration

Abstract submission deadline
20 December 2026
Manuscript submission deadline
20 February 2027
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2374

Topic Information

Dear Colleagues,

Recent breakthroughs in biofabrication are transforming the field of tissue repair and regeneration through the creation of biomimetic constructs that replicate the complexity of native tissue. Advanced techniques—particularly 3D bioprinting, alongside unidirectional freeze-drying, electrospinning, and two-photon lithography—now enable precise control over cell placement, matrix composition, and bioactive cues, producing architectures with tailored mechanical, biochemical, and electrical properties.

The integration of stimuli-responsive nanomaterials, including piezoelectric, plasmonic, and magneto-responsive systems, adds dynamic functionality, converting external stimuli into biochemical signals that regulate cell behavior, modulate inflammation, and accelerate tissue regeneration. This synergy between high-resolution bioprinting and smart nanomaterials is paving the way for adaptive scaffolds capable of on-demand drug delivery, mechanical actuation, and localized bioelectrical stimulation.

This Topic aims to collate cutting-edge research at the intersection of additive manufacturing and stimuli-responsive biomaterials, highlighting the next generation of active, patient-specific constructs poised to redefine regenerative medicine.

Dr. Lorenzo Vannozzi
Dr. Eugenio Redolfi Riva
Topic Editors

Keywords

  • biofabrication
  • tissue repair
  • regenerative medicine
  • 3D bioprinting
  • alongside unidirectional freeze-drying
  • electrospinning
  • two-photon lithography
  • stimuli-responsive biomaterials

 

Participating Journals

Journal Name Impact Factor CiteScore Launched Year First Decision (median) APC
Biomimetics
biomimetics
4.2 6.2 2016 13.5 Days CHF 2200 Submit
Biomolecules
biomolecules
5.6 9.3 2011 16.6 Days CHF 2700 Submit
Biophysica
biophysica
1.8 2.6 2021 19.1 Days CHF 1200 Submit
Cells
cells
6.0 11.4 2012 14.9 Days CHF 2700 Submit
International Journal of Molecular Sciences
ijms
5.6 10.0 2000 17.5 Days CHF 2900 Submit
Materials
materials
3.7 7.0 2008 14.4 Days CHF 2600 Submit
Micro
micro
2.4 4.0 2021 20.4 Days CHF 1200 Submit

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Published Papers (1 paper)

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22 pages, 4637 KB  
Article
The Reconstitution of the Macrophage Niche Reveals Dynamic Transcriptional and Renal Macrophage–Epithelial Communication Networks
by Mohammad Islamuddin, Lixuan Ji, Yilin Chen, Kejing Song, Calder R. Ellsworth, Jack Rappaport, Chenxiao Wang, Shumei Liu, Jay Kolls, Xiaojiang Xu and Xuebin Qin
Cells 2026, 15(12), 1102; https://doi.org/10.3390/cells15121102 - 18 Jun 2026
Viewed by 543
Abstract
Renal-resident macrophages (RMs) are essential regulators of kidney homeostasis and repair, yet the mechanisms governing RM niche regeneration after acute depletion remain poorly defined. To overcome these limitations, we have developed an inducible human CD59- intermedilysin (hCD59-ILY) ablation system, enabling rapid, specific, and [...] Read more.
Renal-resident macrophages (RMs) are essential regulators of kidney homeostasis and repair, yet the mechanisms governing RM niche regeneration after acute depletion remain poorly defined. To overcome these limitations, we have developed an inducible human CD59- intermedilysin (hCD59-ILY) ablation system, enabling rapid, specific, and reversible depletion of targeted macrophage populations, and subsequent replenishment of RMs, followed by longitudinal scRNA-seq analysis of kidneys at baseline and days 1, 3, and 7 post-ablation. RM ablation triggered a rapid and sustained upregulation of Cx3cl1, predominantly in proximal tubular epithelial cells (PTC1/PTC2), establishing a persistent chemotactic niche signal that coincided with macrophage repopulation. Regenerating RMs transitioned from inflammatory/stress-associated states toward metabolically active and proliferative phenotypes enriched in glycolysis, oxidative phosphorylation, MYC, and cell-cycle programs, with attenuation of canonical inflammatory pathways. Cell–cell communication analysis revealed an early burst of intercellular signaling at day 1, followed by progressive normalization, with fibronectin (Fn1), osteopontin (Spp1), chemokine (Ccl), and amyloid precursor protein (App) axes emerging as key mediators of niche restoration. Transcriptional network analysis identified a conserved regulatory module (Tfe3, Mitf, Hif1a, Myc, Gabpa, Rcor1) coordinating macrophage differentiation and regenerative programming, linking metabolic adaptation to lineage reconstitution. Sub-clustering revealed five dynamically shifting RM subsets with distinct inflammatory, remodeling, proliferative, and surveillance states, reflecting a hierarchical regeneration process. Functional validation using clodronate-mediated depletion in Secreted Phosphoprotein 1 (Spp1) (Opn)-deficient mice demonstrated impaired macrophage repopulation, establishing osteopontin as a critical regulator of RM regeneration. Together, these data define a coordinated epithelial–immune circuit in which Cx3cl1-driven chemotaxis, Spp1-dependent signaling, and a core transcriptional network orchestrate macrophage niche reconstitution and kidney repair following acute immune cell ablation. Full article
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