NELL-1: role and mechanisms in disease pathogenesis and development

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

NELL-1 (NEL-like protein 1) is a multifunctional secreted glycoprotein that has been implicated in a variety of biological processes, including skeletal development, immune regulation, and tumorigenesis. Despite its significance, the regulatory mechanisms of NELL-1 across different tissues, the diversity of its signaling pathways, and its context-dependent roles in disease are not fully elucidated. This gap in understanding hinders the systematic development and clinical translation of potential applications. Current research suggests that NELL-1 influences skeletal development and regeneration through pathways such as Wnt/β-catenin, MAPK, and Runx3-Indian hedgehog (Ihh). Additionally, it plays crucial roles in conditions such as membranous nephropathy, various tumors, and neurodevelopmental disorders. The distinct isoforms of NELL-1, such as NELL-1 570 and NELL-1-ΔE, exhibit specific functional properties and hold significant therapeutic promise, particularly in bone regeneration and tumor suppression. This review aims to provide a comprehensive analysis of the molecular mechanisms of NELL-1 in osteogenesis, chondrogenesis, immune regulation, and tumor suppression. It also explores various strategies to enhance its stability and targeting, including PEG modification and nanoparticle delivery systems. In conclusion, NELL-1 represents a key molecule with multi-tissue, multi-dise

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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