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chronic inflammation, promote the secretion of extracellular matrix by fibroblasts and
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the formation of new blood vessels by vascular endothelial cells . Not only that, 3D

printing supports direct loading of mesenchymal stem cells and the construction of
bionic co-culture systems, continuously releasing nutrient factors and further

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optimizing the microenvironment . Lingling Guo et al. loaded the inherent bioactive
components of egg white into hydrogels, thereby providing cell recognition sites,

simulating the extracellular matrix environment, promoting cell adhesion, proliferation

and migration. At the same time, with the help of 3D printing technology, they precisely

constructed the porous structure of hydrogels, enhancing the ability of nutrient

penetration and regulation of cell spatial distribution. Ultimately, this scaffold

significantly accelerated the recovery of cellular function and tissue regeneration in

diabetic wounds through the synergy of biological activity and three-dimensional

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structural characteristics. Similarly, Daniel Rybak et al. embedded electrowoven short
fibers (SFs) loaded with gold nanorods (AuNRs) and dexamethasone (DXM) into

GelMA/SA hydrogels and constructed photothermal responsive scaffolds through 3D

printing. These scaffolds can locally heat up and trigger drug controlled release under
near-infrared light irradiation. Significantly enhance the antibacterial and anti-

inflammatory effects, and promote the adhesion, extension and proliferation of L929

fibroblasts.

The promoting effect of hydrogel on diabetic wound repair had multi-dimensional

biological mechanisms. Its core advantages were not only reflected in the precise

regulation of the wound microenvironment, but also the synergistic repair effect by

targeting the key behaviors of cells. 93-95 In the process of normal skin injury repair,

fibroblasts, as the core effector cells, will quickly respond to the injury signal and

migrate to the wound site to construct a temporary repair hydeogel scaffold by

synthesizing and secreting Col-Ⅰ and other extracellular matrix components. In this

process, the balance between dynamic synthesis and degradation of collagen was the

key to drive orderly tissue repair: matrix metalloproteinases (MMPs) secreted by

fibroblasts and tissue inhibitors (TIMPs) cooperate to regulate collagen turnover,

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