ArticleAdvanced materials (Deerfield Beach, Fla.)2025
Protein-Like Polymers Targeting Keap1/Nrf2 as Therapeutics for Myocardial Infarction.
Article in Advanced materials (Deerfield Beach, Fla.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- An NIR-responsive FeS-loaded alginate hydrogel promotes diabetic wound healing through Nrf2 activation and macrophage polarization.International journal of pharmaceutics: X · 2026Article
- Precise atorvastatin delivery by cardiac homing peptide functionalized nanoliposomes for myocardial damage repair after myocardial infarction.Nanomedicine (London, England) · 2026Article
- Engineering the oxidative myocardium: ROS-responsive biomaterials for precision cardiovascular delivery in ischemia-reperfusion injury and post-infarction remodeling.Frontiers in drug delivery · 2026Review
- 33 Unresolved Questions in Nanoscience and Nanotechnology.ACS nano · 2025Article
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Authors and funding
18 authors.
Funding
Abstract
Myocardial infarction (MI) results in oxidative stress to the myocardium and frequently leads to heart failure (HF). There is an unmet clinical need to develop therapeutics that address the inflammatory stress response and prevent negative left ventricular remodeling. Here, the Keap1/Nrf2 protein-protein interaction is specifically targeted, as Nrf2 activation is known to mitigate the inflammatory response following MI. This is achieved using a Nrf2-mimetic protein-like polymer (PLP) to inhibit the Keap1-Nrf2 interaction. The PLP platform technology provides stability in vivo, potent intracellular bioactivity, and multivalency leading to high avidity Keap1 binding. In vitro and in vivo assays to probe cellular activity and MI therapeutic utility are employed. These Keap1-inhibiting PLPs (Keap1i-PLPs) impart cytoprotection from oxidative stress via Nrf2 activation at sub-nanomolar concentrations in primary cardiomyocytes. Single-digit mg kg
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Registered trials
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