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探索Krüppel样因子在肾脏发育、代谢及疾病中的功能。

Exploring the Functionality of the Krüppel-like Factors in Kidney Development, Metabolism, and Diseases.

作者信息

Salmon-Cabrales Itzel S, de la Garza-Kalife David A, García-González Gabriel, Estrada-Rodríguez Ana E, Jiménez-Gutiérrez Marco Antonio, Santoyo-Suárez Michelle G, Rodríguez-Núñez Oscar, Garza-Treviño Elsa N, Benítez-Chao Diego F, Padilla-Rivas Gerardo R, Islas Jose Francisco

机构信息

Laboratorio de Terapia Celular, Departamento de Bioquímica y Medicina Molecular, Facultad de Medicina, Universidad Autónoma de Nuevo León, Av. Dr. José Eleuterio González 235, Monterrey 64460, Nuevo León, Mexico.

Departmento de Ciencias Básicas, Vicerrectoría de Ciencias de la Salud, Universidad de Monterrey, Ignacio Morones Prieto 4500, Jesus M. Garza, San Pedro Garza García 66238, Nuevo León, Mexico.

出版信息

Life (Basel). 2024 Dec 17;14(12):1671. doi: 10.3390/life14121671.

DOI:10.3390/life14121671
PMID:39768378
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11728015/
Abstract

The kidneys contribute to the overall health of an organism by maintaining systemic homeostasis. This process involves various biological mechanisms, in which the Krüppel-like factors (KLFs), a family of transcription factors, are essential for regulating development, differentiation, proliferation, and cellular apoptosis. They also play a role in the metabolic regulation of essential nutrients, such as glucose and lipids. The dysregulation of these transcription factors is associated with the development of various pathologies, which can ultimately lead to renal fibrosis, severely compromising kidney function. In this context, the present article provides a comprehensive review of the existing literature, offering an enriching analysis of the findings related to the role of KLFs in nephrology, while also highlighting their potential therapeutic role in the treatment of renal diseases.

摘要

肾脏通过维持全身内环境稳定来促进生物体的整体健康。这个过程涉及多种生物学机制,其中,作为一类转录因子的Krüppel样因子(KLFs)对于调节发育、分化、增殖和细胞凋亡至关重要。它们在葡萄糖和脂质等必需营养素的代谢调节中也发挥作用。这些转录因子的失调与各种病理状况的发生发展相关,最终可导致肾纤维化,严重损害肾功能。在此背景下,本文对现有文献进行了全面综述,对与KLFs在肾脏病学中的作用相关的研究结果进行了丰富分析,同时也强调了它们在肾脏疾病治疗中的潜在治疗作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e7a/11728015/aac0156ea95c/life-14-01671-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e7a/11728015/a1de73d105ca/life-14-01671-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e7a/11728015/d5c09d707d2a/life-14-01671-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e7a/11728015/3bb342e7f122/life-14-01671-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e7a/11728015/aac0156ea95c/life-14-01671-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e7a/11728015/a1de73d105ca/life-14-01671-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e7a/11728015/d5c09d707d2a/life-14-01671-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e7a/11728015/3bb342e7f122/life-14-01671-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e7a/11728015/aac0156ea95c/life-14-01671-g004.jpg

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本文引用的文献

1
Podocyte-specific KLF6 primes proximal tubule CaMK1D signaling to attenuate diabetic kidney disease.足细胞特异性 KLF6 激活近端肾小管 CaMK1D 信号通路,从而减轻糖尿病肾病。
Nat Commun. 2024 Sep 13;15(1):8038. doi: 10.1038/s41467-024-52306-5.
2
Krüppel-like factors family in health and disease.健康与疾病中的Krüppel样因子家族。
MedComm (2020). 2024 Sep 10;5(9):e723. doi: 10.1002/mco2.723. eCollection 2024 Sep.
3
Small extracellular vesicles-shuttled miR-23a-3p from mesenchymal stem cells alleviate renal fibrosis and inflammation by inhibiting KLF3/STAT3 axis in diabetic kidney disease.
来自间充质干细胞的小细胞外囊泡转运的 miR-23a-3p 通过抑制糖尿病肾病中的 KLF3/STAT3 轴缓解肾纤维化和炎症。
Int Immunopharmacol. 2024 Sep 30;139:112667. doi: 10.1016/j.intimp.2024.112667. Epub 2024 Jul 16.
4
Lactate drives epithelial-mesenchymal transition in diabetic kidney disease via the H3K14la/KLF5 pathway.乳酸通过 H3K14la/KLF5 通路在糖尿病肾病中的上皮-间充质转化。
Redox Biol. 2024 Sep;75:103246. doi: 10.1016/j.redox.2024.103246. Epub 2024 Jun 20.
5
Is the Cis-Element CACCC-Box a Master Regulatory Element during Cardiovascular Disease? A Bioinformatics Approach from the Perspective of the Krüppel-like Family of Transcription Factors.顺式元件CACCC盒是心血管疾病中的主要调控元件吗?从Krüppel样转录因子家族角度的生物信息学方法。
Life (Basel). 2024 Apr 11;14(4):493. doi: 10.3390/life14040493.
6
Depression of LncRNA DANCR alleviates tubular injury in diabetic nephropathy by regulating KLF5 through sponge miR-214-5p.LncRNA DANCR 的下调通过海绵 miR-214-5p 调控 KLF5 减轻糖尿病肾病肾小管损伤。
BMC Nephrol. 2024 Apr 12;25(1):130. doi: 10.1186/s12882-024-03562-6.
7
KLF transcription factors in bone diseases.KLF 转录因子在骨骼疾病中的作用。
J Cell Mol Med. 2024 Apr;28(8):e18278. doi: 10.1111/jcmm.18278.
8
Intermittent Fasting-Improved Glucose Homeostasis Is Not Entirely Dependent on Caloric Restriction in db/db Male Mice.间歇性禁食改善葡萄糖稳态并不完全依赖于 db/db 雄性小鼠的热量限制。
Diabetes. 2024 Jun 1;73(6):864-878. doi: 10.2337/db23-0157.
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Activation of the YAP/KLF5 transcriptional cascade in renal tubular cells aggravates kidney injury.肾小管细胞中YAP/KLF5转录级联的激活会加重肾损伤。
Mol Ther. 2024 May 1;32(5):1526-1539. doi: 10.1016/j.ymthe.2024.02.031. Epub 2024 Feb 27.
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Krüppel-like factor 4 modulates the miR-101/COL10A1 axis to inhibit renal fibrosis after AKI by regulating epithelial-mesenchymal transition.Krüppel 样因子 4 通过调节上皮-间充质转化来调节 miR-101/COL10A1 轴抑制 AKI 后的肾纤维化。
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