Key Takeaways & Executive Findings
- •• • SA-PBA/E/Sr hydrogel reduced infarct size and increased left ventricular wall thickness, with Masson's staining showing significantly less collagen deposition (blue) compared to MI groups (***P < 0.001), indicating effective mitigation of fibrosis and scar tissue formation. • • The hydrogel promoted macrophage polarization from pro-inflammatory M1 to anti-inflammatory M2 phenotype, decreasing TNF-α secretion and increasing IL-10 production, which is critical for resolving inflammation and fostering a pro-repair microenvironment. • • Incorporation of Sr2+ significantly enhanced endothelial cell migration, a key factor in angiogenesis, leading to accelerated neovascularization in the infarcted tissue, as evidenced by increased vessel density. • • Echocardiographic analysis demonstrated a remarkable increase in ejection fraction and reduced left ventricular dilation, confirming significant cardiac functional recovery after SA-PBA/E/Sr treatment compared to other groups.
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Abstract
Inflammation and ischemic microenvironments represent significant challenges in cardiac repair. To address these issues, a series of dual-dynamically crosslinked alginate-based hydrogels (SA-PBA/E/Sr) containing strontium ions (Sr2+) and epigallocatechin gallate (EGCG) were developed, demonstrating microenvironment modulation and angiogenic capabilities in the myocardial infarction (MI) microenvironment. In the SA-PBA/E/Sr hydrogel system, alginate modified with aminophenylboronic acid (PBA) was synthesized to form boronic acid ester bonds with EGCG and an ionic coordination network with Sr2+ ions. The resulting hydrogel exhibits excellent injectability due to its dual-dynamically crosslinked structure, with its formation and mechanical properties being tunably modulated by the PBA substitution degree, EGCG concentration, and Sr2+ content. The incorporation of EGCG enables the hydrogel to efficiently scavenge reactive oxygen species (ROS) and mitigate oxidative stress-induced cellular damage under hypoxia. Furthermore, the introduction of Sr2+ significantly enhances the migratory capacity of endothelial cells, a critical factor in angiogenesis. In vivo experiments revealed that the injection of SA-PBA/E/Sr hydrogel into the infarcted myocardium of Sprague-Dawley (SD) rats led to reduced ROS levels, alleviated inflammatory responses, suppression of pro-inflammatory M1 macrophage expression, enhancement of anti-inflammatory M2 macrophage expression, and accelerated neovascularization in the damaged tissue. Echocardiographic and histological analyses demonstrated a remarkable increase in ejection fraction and a decreased infarct size, collectively indicating significant cardiac functional recovery.
1. Introduction
Myocardial infarction (MI) remains the leading global cause of mortality, with ischemia-reperfusion injury and subsequent inflammatory cascades driving adverse ventricular remodeling. Current clinical interventions, including reperfusion therapy and pharmacological management, fail to address the complex microenvironmental dysregulation characterized by excessive reactive oxygen species (ROS), persistent inflammation, and impaired angiogenesis. This pathological milieu perpetuates cardiomyocyte apoptosis, fibrosis, and progressive heart failure, underscoring the urgent need for therapies that can simultaneously modulate multiple pathological pathways.
Existing biomaterial strategies, such as antioxidant hydrogels or pro-angiogenic factor delivery, have shown limited efficacy due to insufficient mechanical resilience, rapid clearance, or inability to orchestrate the temporal sequence of repair. The dual-dynamically crosslinked SA-PBA/E/Sr hydrogel addresses these bottlenecks by integrating ROS-scavenging EGCG and pro-angiogenic Sr2+ within a tunable, injectable matrix. The boronic acid ester bonds and ionic coordination networks confer self-healing and shear-thinning properties, enabling minimally invasive delivery and sustained microenvironment regulation. This study systematically evaluates the hydrogel's capacity to attenuate oxidative stress, promote M2 macrophage polarization, and stimulate neovascularization, thereby offering a synergistic platform for cardiac repair.
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ZHANG Haitao, LIANG Lei, YUE Zhiwei, WANG Chengyao, CHEN Linyu, LU Jiajun, ZHANG Hong, YAO Fanglian, SUN Hong, LI Junjie (2025). A Dual-Dynamically Crosslinked Hydrogel for Cardiac Repair with Microenvironment Regulation and Angiogenic Functions. SCIENCE CHINA Materials. https://doi.org/10.1007/s40843-025-3619-1
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Frequently Asked Questions
What is the quantitative evidence for reduced infarct size and fibrosis after SA-PBA/E/Sr treatment?
Masson's staining revealed significantly less collagen deposition (blue) in the SA-PBA/E/Sr group compared to MI controls, with statistical significance at ***P < 0.001. Sirius Red staining corroborated these findings, showing a significant reduction in red collagen signal and an increase in yellow normal tissue signal, indicating alleviated fibrosis.
How does the dual-dynamic crosslinking affect the injectability and mechanical properties of the hydrogel?
The dual-dynamically crosslinked structure, formed by boronic acid ester bonds between PBA-modified alginate and EGCG, and ionic coordination with Sr2+, confers excellent injectability and tunable mechanical properties. The hydrogel's formation and mechanics can be modulated by PBA substitution degree, EGCG concentration, and Sr2+ content, allowing customization for cardiac tissue compatibility.
What is the mechanism by which Sr2+ enhances angiogenesis, and what are the observed effects?
Sr2+ significantly enhances endothelial cell migration, a critical factor in angiogenesis. In vivo, this led to accelerated neovascularization in the infarcted myocardium, as evidenced by increased vessel density and improved perfusion, contributing to cardiac functional recovery.
Does the hydrogel modulate macrophage polarization, and what are the cytokine changes?
Yes, SA-PBA/E/Sr hydrogel promotes macrophage polarization from pro-inflammatory M1 to anti-inflammatory M2 phenotype. This shift decreases secretion of pro-inflammatory cytokines (e.g., TNF-α) and increases anti-inflammatory cytokines (e.g., IL-10), thereby mitigating inflammation and fostering a pro-repair microenvironment.
What are the limitations or potential translational challenges for this hydrogel?
While the study demonstrates efficacy in a rat MI model, long-term degradation, immune response, and scalability for human use require further investigation. The optimal balance of PBA substitution, EGCG, and Sr2+ concentrations for human cardiac tissue, as well as manufacturing under GMP conditions, must be established.
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