Engineering Catalytic Biomaterials for Cellular Fate Modulation

ABSTRACT Regulated cell death is a fundamental determinant of tissue homeostasis, immune surveillance, and disease progression. However, its therapeutic manipulation requires precise spatiotemporal and pathway‐selective control. Beyond apoptosis, diverse inflammatory, metabolic, and immunogenic death programs are governed by interconnected redox, metabolic, ionic, and inflammatory networks. Here, we highlight catalytic biomaterials as emerging platforms for reprogramming cell fate through the direct manipulation of these biochemical networks. By converting disease‐associated endogenous cues or externally supplied energy into localized chemical outputs, including reactive species, metal ions, metabolic intermediates, and immunogenic signals, catalytic biomaterials can intervene at critical biochemical nodes that determine cellular survival, death, and immune consequences. Through enzyme‐mimetic, Fenton‐like, photo‐, sono‐, radio‐, and cascade catalysis, these materials enable bidirectional and context‐dependent control, selectively inducing tumor cell death while protecting vulnerable tissues from pathological cell loss. We discuss how material structure, catalytic activity, microenvironmental responsiveness, external stimuli, and subcellular targeting collectively shape cell fate outcomes across major cell death modalities. Finally, we highlight emerging opportunities and challenges in establishing predictive structure‐activity‐fate relationships, real‐time catalytic monitoring, mechanistic elucidation, biosafety, and clinical translation, outlining a path toward programmable catalytic regulation of cell fate.

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Publication Details

Journal
Angewandte Chemie Novit
Published
2026-11-04
DOI
https://doi.org/10.1002/anov.70040
Primary Topic
Nanoplatforms for cancer theranostics
Type
article
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article

Engineering Catalytic Biomaterials for Cellular Fate Modulation

Chenyao Wu, Wei Feng, Yu Chen, Jiayi Gu et al.
Angewandte Chemie Novit
Nanoplatforms for cancer theranostics
article

Engineering Catalytic Biomaterials for Cellular Fate Modulation

Chenyao Wu, Wei Feng, Yu Chen, Jiayi Gu, Baoying Xu
article en

Abstract

ABSTRACT Regulated cell death is a fundamental determinant of tissue homeostasis, immune surveillance, and disease progression. However, its therapeutic manipulation requires precise spatiotemporal and pathway‐selective control. Beyond apoptosis, diverse inflammatory, metabolic, and immunogenic death programs are governed by interconnected redox, metabolic, ionic, and inflammatory networks. Here, we highlight catalytic biomaterials as emerging platforms for reprogramming cell fate through the direct manipulation of these biochemical networks. By converting disease‐associated endogenous cues or externally supplied energy into localized chemical outputs, including reactive species, metal ions, metabolic intermediates, and immunogenic signals, catalytic biomaterials can intervene at critical biochemical nodes that determine cellular survival, death, and immune consequences. Through enzyme‐mimetic, Fenton‐like, photo‐, sono‐, radio‐, and cascade catalysis, these materials enable bidirectional and context‐dependent control, selectively inducing tumor cell death while protecting vulnerable tissues from pathological cell loss. We discuss how material structure, catalytic activity, microenvironmental responsiveness, external stimuli, and subcellular targeting collectively shape cell fate outcomes across major cell death modalities. Finally, we highlight emerging opportunities and challenges in establishing predictive structure‐activity‐fate relationships, real‐time catalytic monitoring, mechanistic elucidation, biosafety, and clinical translation, outlining a path toward programmable catalytic regulation of cell fate.

Angewandte Chemie NovitVol. 2(4)
Shanghai University (CN)
Openalex Percentile: Top 26%
Nanoplatforms for cancer theranostics
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Engineering Catalytic Biomaterials for Cellular Fate Modulation — Chenyao Wu, Wei Feng, et al. · Angewandte Chemie Novit (2026) | TGRS Research Map | TGRS