解码和理解分子机制:细胞信号通路、胰岛β细胞再生和干细胞龛位工程治疗糖尿病

Rajiv Kumar, Gerardo Caruso
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摘要

干细胞生物工程通过将先进技术应用于干细胞衍生系统,解决再生医学和细胞疗法问题。尽管干细胞应用前景广阔,但由于知识不全,干细胞应用受到限制。干细胞和植物化学物质通过阻止β细胞退化和促进内源性胰岛再生,显示出治疗糖尿病的潜力。目前的糖尿病细胞疗法包括干细胞、成熟的胰腺细胞、内分泌祖细胞和β细胞,研究人员正在积极寻找临床相关β细胞的新细胞来源。干细胞衍生的胰腺细胞尤其有望用于胰岛再生。糖尿病源于细胞丢失或功能失调:1 型糖尿病源于自身免疫损伤,而 2 型糖尿病则主要归因于细胞功能失调或胰岛素抵抗。唯一的手术疗法是胰岛移植,但必须终生抑制免疫。成人β细胞再生治疗策略已取得重大进展。本综述评估了与β细胞存活和增殖有关的细胞信号通路研究,探讨了胰岛替代或再生的再生医学方法。置换 "技术涉及细胞移植,而 "再生 "策略则通过复制保存细胞群。此外,蒿甲醚和γ-氨基丁酸可诱导胰腺细胞形成β细胞样表型,从而有可能帮助开发新的β细胞样细胞,用于治疗大鼠的严重糖尿病。了解G蛋白偶联受体激活途径至关重要,因为胰岛素依赖型糖尿病的新治疗策略可能会从这些知识中产生。
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Decoding and understanding molecular mechanisms: Cell signaling pathways, pancreatic β-cell regeneration, and stem cell niche engineering for diabetes
Stem cell bioengineering addresses regenerative medicine and cellular therapies by applying advanced techniques to stem-cell-derived systems. Despite their promise, stem cell applications are limited by incomplete knowledge. Stem cells and phytochemicals show potential in treating diabetes by halting β-cell degeneration and promoting endogenous islet regeneration. Current diabetes cell therapies include stem cells, mature pancreatic cells, endocrine progenitors, and β-cells, with researchers actively seeking new cell sources for clinically relevant β-cells. Stem cell-derived pancreatic cells are particularly promising for pancreatic islet regeneration. Diabetes mellitus results from cell loss or malfunction: Type 1 diabetes stems from autoimmune damage, whereas Type 2 diabetes is largely attributed to cell malfunction or insulin resistance. The only operative therapy, islet transplantation, necessitates lifelong immune suppression. Significant progress has been made in strategies for therapeutic adult β-cell regeneration. This review assesses studies on cellular signaling pathways linked to β-cell survival and proliferation, exploring regenerative medicine methodologies for pancreatic islet replacement or regeneration. While the “replacement” technique involves cell transplantation, the “regeneration” strategy preserves cell populations through replication. Moreover, artemether and gamma-aminobutyric acid induce pancreatic cells to adopt β-cell-like phenotypes, potentially aiding in the development of new β-cell-like cells for treating severe diabetes in rats. Understanding G-protein-coupled receptor activation pathways is crucial, as new treatment strategies for insulin-dependent diabetic mellitus may emerge from this knowledge.
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