Ask about this productRelated genes to: HIF1A protein
- Gene:
- HIF1A NIH gene
- Name:
- hypoxia inducible factor 1 subunit alpha
- Previous symbol:
- -
- Synonyms:
- MOP1, HIF-1alpha, PASD8, HIF1, bHLHe78
- Chromosome:
- 14q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-27
- Date modifiied:
- 2018-04-23
Related products to: HIF1A protein
Related articles to: HIF1A protein
- Neuroinflammation plays a crucial role in various central nervous system (CNS) disorders. This study aims to investigate the potential neuroprotective effects of radiofrequency electromagnetic fields (RF-EMF) and pulsed magnetic fields (PMF) on oxidative stress, apoptosis, and neuroinflammation in lipopolysaccharide (LPS)-induced acute neuroinflammation model in rats. - Source: PubMed
Publication date: 2026/05/25
Bindal AhmetAsci HalilAsci SanemTepebasi Muhammet YusufIlhan IlterOzmen OzlemComlekci Selcuk - Di (2-ethylhexyl) phthalate (DEHP), a ubiquitous environmental plasticizer, is increasingly linked to neurotoxicity and carcinogenesis. However, its role in glioma pathogenesis remains poorly understood. This study integrates network toxicology and machine learning to identify molecular targets of DEHP in glioma. - Source: PubMed
Publication date: 2026/05/08
Li RenRen ChaominHe LuWang ShuleGuo Geng - Chinese herbal medicine has a long history of treating insomnia with excellent curative effects; however, the underlying mechanisms remain unclear. This study discusses the mechanism and curative effects of the main Chinese herbal medicines in the Bushen Anzhi recipe for managing aging-related insomnia (ARI). - Source: PubMed
Publication date: 2026/05/08
Li HaimingLiang RuiningLi ZhenhuiCui WenjunHu YanlingZuo GuangkeZhu HailongZhang Xingping - Androgenetic alopecia (AA) is a common condition that is characterized by androgen-induced follicular miniaturization and abnormal hair cycling, against which there are as yet no effective therapeutic interventions. The current study outlines the possibility of using stigmasterol (STR) as a therapeutic agent of AA, using geometry optimization, network pharmacology, molecular docking, and molecular dynamics (MD) simulations. Geometry optimization was done using the PM3 Hartree-Fock protocol, and the most stable conformation of STR was found with a total electronic energy of -164.36 au. The integrative gap analysis of target interactions presented sixty-three common genes in the target interaction between STR pharmacodynamics and AA pathogenesis. Ten core genes (AR, CDK4, ESR1, ESR2, HIF1A, MAPK3, MDM2, NR3C1, PGR, PPARG) were subsequently chosen in order to highlight the mechanistic nature of AA. Specifically, AR mediates androgenic signaling, which triggers the follicular miniaturization; ESR1 and ESR2 affect the cutaneous hair cycling and inflammatory cascades, and MAPK3 coordinates the inflammatory and apoptotic pathways. Docking studies revealed a strong binding of STR with all the hub genes, with the strongest binding affinity against MAPK3 (-9.1 kcal/mol) being observed compared to the binding energy of finasteride (-8.6 kcal/mol). Evidence of the thermodynamic stability of the STR-MAPK3 complex was found by MD simulations over 200 nanoseconds. Taken together, these results support the ability of STR to regulate a variety of AA-related mechanisms and thus predetermine it as one of the most promising natural therapeutic agents. However, further empirical confirmation is mandatory to unify the prospective application of STR in the clinical treatment of AA. - Source: PubMed
Publication date: 2026/05/23
Otuokere Ifeanyi EdozieNgwu Comfort MichaelIheanyichukwu Julian IbejiMac-Kalunta Onuchi MarygemNwadire Felix ChigozieNwankwo Chinedum IfeanyiEgbucha Joy NUfearoh Stella MbanyeakuChukwuemeka-Okorie Helen OUzoma Nwokoma EsomchiOluwaseyi Adeniji Moshood - This study evaluated neuroprotective potential of an oxazolidine derivative, (4-(4-methoxyphenyl)-3-(4-nitrophenyl)-1,2-oxazolidine) (named AP9), and its chitosan (Ch) nanoparticle formulation (AP9-Ch), utilizing an integrated in silico, in vitro, and in vivo zebrafish model. Network pharmacology and molecular docking identified AP9 as a lead chemical with high affinity for hub proteins: as AKT1, EGFR, ESR1, HIF1A, MTOR, and PARP1, implying an involvement in neurodegenerative disease pathways. In vitro tests showed that AP9 inhibited acetylcholinesterase by 85.85% at 100 μM, a level similar to that of galantamine. Nanoparticle analysis revealed a spherical morphology, reduced crystallinity, and effective conjugation, suggesting improved drug stability and release potential. Toxicity tests on zebrafish embryos revealed that AP9 was well tolerated up to 150 μM, with few developmental abnormalities. Behavioral assays showed that AP9-Ch reduced BPA-induced anxiety-like behavior, aggression, and cognitive impairment, as demonstrated by improved performance in open field, novel tank diving, mirror biting, and T-maze testing. Biochemical tests showed that antioxidant defenses were restored and lipid peroxidation was reduced, while histology revealed protection of brain cytoarchitecture. Gene expression investigations revealed downregulation of NF-κB, COX-2, and TNF-α, and overexpression of BDNF. Overall, these findings indicate that AP9-Ch is a promising multimodal neuroprotective drug with cholinesterase-inhibitory, antioxidant, and anti-inflammatory properties. - Source: PubMed
Publication date: 2026/05/23
Ramya Ranjan Nayak S PHerold AveedaMohammed VajagathaliChinnasamy ManojPalaniappan SenthilkumarAlmutairi Bader OAlmutairi Mikhlid HChoi Ki ChoonArokiyaraj SelvarajValan Arasu MariadhasMuthu Kumaradoss KathiravanArockiaraj Jesu