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Last update 08 May 2025

KLF2

Last update 08 May 2025

Basic Info

Synonyms

KLF2, Krueppel-like factor 2, Kruppel like factor 2

+ [2]

Introduction

Transcription factor that binds to the CACCC box in the promoter of target genes such as HBB/beta globin or NOV and activates their transcription (PubMed:21063504). Might be involved in transcriptional regulation by modulating the binding of the RARA nuclear receptor to RARE DNA elements (PubMed:28167758).

Drugs associated with KLF2

US20250109143

Patent Mining

Target

KLF2

Mechanism-

Active Org.

Riparian Pharmaceuticals, Inc. [+1]

Originator Org.

Pfizer Inc. [+1]

Active Indication

Autoimmune Diseases [+5]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

CN118974057

Patent Mining

Target

KLF2

Mechanism-

Active Org.

Riparian Pharmaceuticals, Inc.

Originator Org.

Riparian Pharmaceuticals, Inc.

Active Indication

Cardiovascular Diseases [+2]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

CN114591282

Patent Mining

Target

KLF2

Mechanism-

Active Org.

Institute of Medicinal Biotechnology Academy of Medical Scien [+1]

Originator Org.

Institute of Medicinal Biotechnology Academy of Medical Scien [+1]

Active Indication

Cardiovascular Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with KLF2

100 Translational Medicine associated with KLF2

0 Patents (Medical) associated with KLF2

1,216

Literatures (Medical) associated with KLF2

01 Dec 2025·Histochemistry and Cell Biology

Modulation of placental angiogenesis by metformin in a rat model of gestational diabetes

Article

Author: Eldakhakhny, Basmah M ; Elsamanoudy, Ayman Z ; Almoghrabi, Yousef M ; Mohie, Passant M ; Elfattah, Amany A Abd ; El-Khair, Salwa M Abo ; Ghoneim, Fatma M ; Hassan, Fatma E ; Soliman, Mona F M

Gestational diabetes mellitus (GDM) significantly disrupts placental structure and function, leading to complications such as intrauterine growth restriction (IUGR) and preeclampsia. This study aimed to investigate the effects of GDM on placental histology, angiogenesis, and oxidative stress, as well as evaluate metformin's protective role in mitigating these changes. A total of 60 pregnant Sprague-Dawley rats were divided into four groups: control, metformin-treated, GDM, and GDM with metformin. GDM was induced using streptozotocin (STZ) at 40 mg/kg, and metformin was administered at 200 mg/kg from gestational day (GD) 4 to GD17. Blood glucose and insulin levels were assessed, and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) was calculated. Placentae were weighed and subjected to histological, immunohistochemical, and molecular analyses, focusing on key angiogenesis markers (VEGF, VEGFR, CD31, KLF2) and oxidative stress indicators (MDA, eNOS). GDM increased placental weight, angiogenesis (elevated VEGF, VEGFR, CD31), and oxidative stress (elevated MDA, eNOS). Histopathological changes included villous edema, membrane rupture, and hemosiderin deposition. Metformin treatment reduced placental weight; normalized VEGF, KLF2, and PlGF expression; and improved placental architecture. Additionally, oxidative stress was significantly reduced in metformin-treated GDM rats. In conclusion, GDM induces placental abnormalities, promoting excessive angiogenesis and oxidative stress, potentially leading to IUGR and other complications. Metformin showed protective effects by reducing placental overgrowth and restoring vascular and oxidative balance. These findings suggest that metformin may play a therapeutic role in improving placental health in GDM pregnancies, warranting further investigation into its long-term effects on fetal development and maternal health.

01 Jun 2025·International Dental Journal

KLF2 Promotes Osteogenic Differentiation of Human Periodontal Ligament Stem Cells by Regulating Nrf2 Expression

Article

Author: Deng, Lichao ; Chen, Jiujiu

OBJECTIVEPeriodontal ligament stem cells (PDLSCs) are emerging as a promising source for periodontal regeneration and to manage periodontitis. This study aims to investigate the roles of Krüppel-like factor 2 (KLF2) and nuclear factor erythroid 2-related factor (Nrf2) in mediating osteogenic differentiation of human PDLSCs (hPDLSCs) in the context of lipopolysaccharide (LPS) stimulation.METHODSThe osteogenic differentiation potential of hPDLSCs isolated from human premolar root samples were examined by alkaline phosphatase (ALP) staining and ALP activity assay, Alizarin red S staining and quantitative analysis of mineralised matrix. Intracellular reactive oxygen species (ROS) production and glutathione (GSH) concentration were assessed to reflect oxidative stress.RESULTSKLF2 overexpression influenced Nrf2-regulated transcription, leading to significant increases in GSH concentration, ALP activity, mineralised matrix formation, and RUNX2 expression in LPS-stimulated hPDLSCs, as well as significant reductions in ROS production and cell apoptosis. The subsequent Nrf2 knockdown impaired the protective effect of KLF2 on hPDLSCs against LPS stimulation.CONCLUSIONThe findings of the study demonstrate KLF2 overexpression has the ability to promote the osteogenic differentiation of hPDLSCs by promoting Nrf2 activation, suggesting that KLF2 mediating Nrf2 could be a promising target to facilitate the efficacy of PDLSC-based bone regeneration in periodontitis.

05 May 2025·Journal of Experimental Medicine

KLF2 expression in IgG plasma cells at their induction site regulates the migration program

Article

Author: Koike, Takuya ; Kawakami, Ryoji ; Ise, Wataru ; Kuwabara, Mana ; Ichiyama, Kenji ; Shiroguchi, Katsuyuki ; Yamamoto, Hiromi ; Tai, Yuki ; Shirai, Taiichiro ; Shimada, Nozomi ; Inoue, Takeshi ; Kurosaki, Tomohiro ; Kawai, Chie ; Shida, Kyoko ; Sakaguchi, Shimon ; Suzuki, Kazuhiro ; Hojo, Nozomi

Newly generated plasma cells in secondary lymphoid organs migrate to niches in the bone marrow, wherein they survive as long-lived plasma cells (LLPCs). Although LLPCs have been extensively characterized, it is still unclear what the key determinant(s) are for plasma cell longevity. One model postulates that plasma cell heterogeneity is established at the induction site, thereby instructing their longevity. Here, we found that, among newly generated IgG plasma cells, integrin β7hi marks plasma cells predisposed to home to the bone marrow, whereas integrin β7lo cells remain in secondary lymphoid organs. Mechanistically, this egress-prone fraction had a higher expression of the KLF2 transcription factor, the loss of which resulted in defective egress by downregulating S1PR1 and CD11b. Disruption of plasma cell egress results in defective antibody durability, thereby making mice more susceptible to influenza reinfection. Thus, the migration program of plasma cells established at the induction site plays a critical role in determining antibody durability.

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KLF2

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