NFKB1 x Nrf2

Last update 08 May 2025

Basic Info

Related Targets

NFKB1Nrf2

Drugs associated with NFKB1 x Nrf2

AQP-1180

Target

NFKB1 x Nrf2

Mechanism

NFKB1 modulators [+1]

Active Org.-

Originator Org.

Aquapharm Biodiscovery Ltd.

Active Indication-

Inactive Indication

Inflammation

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with NFKB1 x Nrf2

100 Translational Medicine associated with NFKB1 x Nrf2

0 Patents (Medical) associated with NFKB1 x Nrf2

288

Literatures (Medical) associated with NFKB1 x Nrf2

01 May 2025·Environment International

Deoxynivalenol exposure-related male reproductive toxicity in mammals: Molecular mechanisms, detoxification and future directions

Review

Author: Hao, Zhihui ; Wang, Zhanhui ; Liu, Dingkuo ; Velkov, Tony ; Conti, Gea Oliveri ; Shen, Jianzhong ; Dai, Chongshan

An increasing body of evidence indicates that exposure to widespread, environmental and food contaminants such as mycotoxins may cause endocrine disorders and infertility. Deoxynivalenol (DON), which is a toxic secondary metabolite produced by Fusarium fungi, can lead to multiple harmful effects in humans and animals, such as hepatotoxicity, nephrotoxicity, immunotoxicity, gastrointestinal toxicity, neurotoxicity, genetic toxicity and carcinogenicity. Recently, there has been growing concern about DON-induced male infertility. Exposure to DON and its metabolites can damage the structure and function of male reproductive organs, resulting in impairment of gametogenesis and thus impaired fertility. Potential molecular mechanisms involve oxidative stress, inflammatory response, mitochondrial dysfunction, apoptosis, cell cycle arrest, pyroptosis, and ferroptosis. Moreover, several signaling pathways, including nuclear factor-kappa B, mitogen-activated protein kinase, NLR family pyrin domain containing 3, nuclear factor erythroid 2-related factor 2, AMP-activated protein kinase, mitochondrial apoptotic pathways, and microRNAs are involved in these detrimental biological processes. Research has shown that several antioxidants, small-molecule inhibitors, or proteins (such as lactoferrin) supplementation can potentially offer protective effects by targeting these signaling pathways. This review comprehensively summarizes the harmful effects of DON exposure on male reproductive function in mammals, the underlying molecular mechanisms and emphasizes the potential of several small molecules as protective therapeutics. In the further, the systematic risk assessment when DON at environmental exposure doses to human reproductive health, the in-depth and precise molecular mechanism investigation using emerging technologies, and the development of more effective intervention strategies warrant urgent investigation.

01 Apr 2025·Computational Biology and Chemistry

Exploring immune gene expression and potential regulatory mechanisms in anaplastic thyroid carcinoma using a combination of single-cell and bulk RNA sequencing data

Article

Author: Shang, Jinbiao ; Zhou, Kehui ; Zhang, Shijia ; Lan, Xiabin

Thyroid cancer includes papillary thyroid carcinoma (PTC) and anaplastic thyroid carcinoma (ATC). While PTC has an excellent prognosis, ATC has a dismal prognosis, necessitating the identification of novel targets in ATC to aid in ATC diagnosis and treatment. Therefore, we analyzed ATC single-cell RNA sequencing (scRNA-seq) and bulk RNA sequencing (bulk RNA-seq) data from the Gene Expression Omnibus (GEO), retrieved immune-related genes from the ImmPort database, and identified differentially expressed immune genes within single-cell subgroups. The AUCell package in R was used to calculate activity scores for single-cell subgroups and identify active cell populations. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were performed on differentially expressed genes (DEGs) in active cell populations. Then, we integrated thyroid-cancer scRNA-seq and bulk RNA-seq data to identify overlapping DEGs. Relevant transcription factors (TFs) were retrieved from the TRRUST database. A protein-protein interaction (PPI) network for key TFs was created using the STRING database. Simultaneously, drugs associated with key TFs were obtained from DGIdb. ScRNA-seq cluster analysis showed that T/natural killer (NK) cells were more distributed in ATC and that thyrocytes cells were more distributed in PTC. We obtained 264 differential immune genes (DIGs) from the IMMPORT database and integrated scRNA-seq cluster analysis to identify the active cell T/NK cells and myeloid cells. Integrated bulk RNA-seq analysis obtained common immune genes (CIGs) such as TMSB4X, NFKB1, TNFRSF1B, and B2M. The nine CIG-related TFs (CEBPB, SPI1, NFKB1, RUNX1, NFE2L2, REL, CIITA, KLF6, and CEBPD) in myeloid cells and three TFs (NFKB1, FOXO1, and NR3C1) in T/NK cells were obtained from the TRRUST database. The key genes we identified represent potential targets for treating ATC.

01 Mar 2025·Journal of Food Science

Lentinan alleviates cadmium‐induced kidney injury by reducing cadmium accumulation via promoting cadmium excretion and metallothionein synthesis and regulating silencing information regulator1/nuclear factor erythroid 2–related factor 2/nuclear factor kappa‐B signaling pathway

Article

Author: Wang, Yinping ; Wang, Dongxu ; Gan, Ren‐You ; Shen, Yue ; Wang, Shiqiong ; Wang, Xiaoxiao ; Li, Ning ; Qiao, Mingwu ; Huang, Xianqing ; Hu, Mei ; Zhao, Qiuyan ; Song, Lianjun ; Li, Qian ; Zhao, Guangshan

AbstractCadmium (Cd) is a widely distributed environmental heavy metal pollutant. It is extremely toxic to the kidney. This study investigated the potential mechanisms of action of lentinan (LNT), a fungal polysaccharide, on protecting against Cd‐induced kidney injury in mice. Male Kunming mice were administered with CdCl2 (2.5 mg/kg/b.w.) by intragastric gavage and LNT in drinking water (1 mg/mL) for 10 weeks. Histological examination revealed that LNT reduced the glomerular atrophy, lymphocyte infiltration, tubular congestion, and collagen accumulation caused by Cd exposure. However, oral administration of LNT decreased Cd levels in kidney by promoting the excretion of Cd in feces and increasing the production of metallothionein (MT) in the kidney. In addition, LNT treatment alleviated Cd‐induced kidney excessive mitophagy by upregulating silencing information regulator1 (SIRT1) and prevented subsequent oxidative stress and inflammatory responses by upregulating nuclear factor erythroid 2–related factor 2 (Nrf2) and downregulating nuclear factor kappa‐B (NF‐κB) signaling pathways. Further, the protein expression levels of profibrotic factors, including Tgf‐β1, alpha smooth muscle actin, and collagen type I alpha 1 chain, and the progression of fibrosis, were significantly reduced in the kidneys of mice treated with LNT. Collectively, our findings suggest that LNT can relieve the nephrotoxicity of Cd by decreasing its accumulation via promoting Cd excretion and MT synthesis and regulating the SIRT1/Nrf2/NF‐κB signaling pathway.

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