Deng Kaicheng, Hua Yuyan, Gao Ying, Zheng Houwei, Jiang Yangzi, Wang Yaping, Gao Changyou, Ren Tanchen, Zhu Yang
State Key Laboratory of Transvascular Implantation Devices, Department of Cardiology of The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.
MOE Key Laboratory of Macromolecular Synthesis and Functionalization, Department of Polymer Science and Engineering, Zhejiang University, Hangzhou, 310027, China.
Adv Sci (Weinh). 2024 Nov;11(43):e2408013. doi: 10.1002/advs.202408013. Epub 2024 Sep 23.
HIF-1α (hypoxia induced factor-1α), a vital protective signal against hypoxia, has a short lifetime after myocardial infarction (MI). Increasing HIF-1α stability by inhibiting its hydroxylation with prolyl hydroxylases inhibitors such as DPCA (1,4-dihydrophenonthrolin-4-one-3-carboxylic acid) presents positive results. However, the optimal inhibitor administration profile for MI treatment is still unexplored. Here, injectable, thermosensitive hydrogels with programmable DPCA release are designed and synthesized. Hydrogel degradation and slow DPCA release are coupled to form a feedback loop by attaching pendant DPCA to polymer backbone, which serve as additional crosslinking points through π-π and hydrophobic interactions. Pendant carboxyl groups are added to the copolymer to accelerate DPCA release. Burst release in the acute phase for myocardial protection and extended near zero-order release across the inflammatory and fibrotic phases with different rates are achieved. All DPCA-releasing hydrogels upregulate HIF-1α, decrease apoptosis, promote angiogenesis, and stimulate cardiomyocyte proliferation, leading to preserved cardiac function and ventricular geometry. Faster hydrogel degradation induced by faster DPCA release results in a HIF-1α expression eight times of healthy control and better therapeutic effect in MI treatment. This research demonstrates the value of precise regulation of HIF-1α expression in treating MI and other relevant diseases and provides an implantable device-based modulation strategy.
缺氧诱导因子-1α(HIF-1α)是一种重要的抗缺氧保护信号,在心肌梗死(MI)后寿命较短。用脯氨酰羟化酶抑制剂如DPCA(1,4-二氢菲咯啉-4-酮-3-羧酸)抑制其羟基化来提高HIF-1α的稳定性已取得积极成果。然而,用于MI治疗的最佳抑制剂给药方案仍未被探索。在此,设计并合成了具有可编程DPCA释放功能的可注射热敏水凝胶。通过将侧链DPCA连接到聚合物主链上,使水凝胶降解和DPCA缓慢释放形成反馈回路,DPCA通过π-π和疏水相互作用作为额外的交联点。向共聚物中添加侧链羧基以加速DPCA释放。实现了急性期的突发释放以保护心肌,并在炎症期和纤维化期以不同速率实现接近零级的延长释放。所有释放DPCA的水凝胶均上调HIF-1α、减少细胞凋亡、促进血管生成并刺激心肌细胞增殖,从而保留心脏功能和心室形态。更快的DPCA释放诱导更快的水凝胶降解,导致HIF-1α表达是健康对照的八倍,在MI治疗中具有更好的治疗效果。本研究证明了在治疗MI和其他相关疾病中精确调节HIF-1α表达的价值,并提供了一种基于可植入装置的调节策略。