Ask about this productRelated genes to: PFKFB3 antibody
- Gene:
- PFKFB3 NIH gene
- Name:
- 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 10p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-01-29
- Date modifiied:
- 2015-09-04
Related products to: PFKFB3 antibody
Related articles to: PFKFB3 antibody
- Acute respiratory distress syndrome (ARDS) is a life-threatening condition with high mortality and limited effective pharmacotherapies. Accumulating evidence has established mitochondrial dysfunction as a central pathogenic hub in ARDS. Injured mitochondria exhibit excessive reactive oxygen species production, impaired mitophagy, aberrant dynamics (predominantly Drp1-mediated fission), reduced biogenesis, and release of mitochondrial DNA as a damage-associated molecular pattern. These alterations trigger inflammatory cascades via the cGAS/STING and NLRP3 pathways, while simultaneously driving a metabolic shift from oxidative phosphorylation to aerobic glycolysis, the Warburg effect. Key glycolytic enzymes, including PKM2, PDK4, GAPDH, and PGK1, reinforce mitochondrial damage through lactate production and HIF-1α stabilization, creating a vicious cycle. Notably, PFKFB3 exhibits cell-type-specific duality, exerting protective effects in alveolar epithelial cells while promoting NETosis in neutrophils. Distinct cell types in the lung, alveolar macrophages, neutrophils, alveolar epithelial cells, and pulmonary endothelial cells exhibit unique mitochondrial and metabolic alterations that collectively perpetuate injury and impair repair. Therapeutically, mitochondria-targeted agents (MitoQ, MOTS-c), modulators of mitochondrial dynamics (baicalein, hydrogen), inhibitors of glycolytic enzymes (PFKFB3, PKM2, PDK4), natural compounds (1-octyl itaconate, shikonin, scutellarin), and mesenchymal stromal cell-mediated mitochondrial transfer have shown promise in preclinical models. This review synthesizes current understanding of the regulatory mechanisms linking mitochondrial dysfunction and metabolic reprogramming in ARDS, discusses cell-type-specific contributions, and highlights emerging therapeutic strategies. Targeting mitochondrial homeostasis and the associated glycolytic shift may offer a transformative approach to ARDS treatment, though challenges related to cell specificity, safety, and clinical translation remain. - Source: PubMed
Publication date: 2026/07/29
Li Yu-HuanWang MiaoWan KeLi JunLi Xiao-Feng - Parabens are antimicrobial preservatives with endocrine-disrupting potential. Because methylparaben (MeP), ethylparaben (EtP), and butylparaben (BuP) differ in alkyl-chain length and biological potency, their comparison may reveal structure-dependent cellular responses. Using K562 chronic myeloid leukemia cells, we compared the effects of MeP, EtP, and BuP on cytotoxicity, metabolic activity assessed by resazurin reduction, proliferation- and stress-related markers, and WNT/β-catenin- and PPARγ-associated signaling. Cells were exposed to MeP, EtP, or BuP for 24 or 48 h; pathway-focused experiments used 1 μM parabens alone or with methyl 3-{[(4-methylphenyl)sulfonyl]amino}benzoate (MSAB), a β-catenin-directed WNT/β-catenin inhibitor, or GW9662, a PPARγ antagonist. MeP did not significantly affect LDH release or resazurin reduction. In contrast, EtP and BuP increased resazurin reduction at nanomolar and low-micromolar concentrations. At 1 μM, this response was not accompanied by marked LDH release, ROS generation, or cell-cycle alterations and therefore did not indicate overt acute cytotoxicity or robust proliferation. This response was accompanied by increased expression of WNT-related and glycolysis-associated genes, including AXIN2, LEF1, SLC2A1, HK2, PDK1, and PFKFB3. Parabens also induced divergent c-MYC regulation, with decreased c-MYC mRNA but increased protein abundance, and modulated PPARγ-associated signaling, antioxidant enzymes, caspase-related responses, and p-p62-related signaling. MSAB and GW9662 modified the resazurin-reduction response; however, these pharmacological effects did not establish direct β-catenin or PPARγ dependence. Overall, EtP and BuP, particularly BuP, produced stronger effects than MeP on resazurin reduction and several WNT/β-catenin-, PPARγ-, and p-p62-associated readouts. - Source: PubMed
Publication date: 2026/08/12
Szychowski Konrad ASkóra Bartosz - Phellodendri Chinensis Cortex (PCC), a classic herb for "clearing heat and drying dampness," is traditionally used to treat gout and uric acid nephropathy (UAN) for its urate-lowering and nephroprotective properties. Yet, the mechanism of its direct renoprotective effect remains unclear. - Source: PubMed
Publication date: 2026/08/12
Li XinyiLuo QingLi ZikangLi QiuxianLu XiaoweiChen ManruWang XinhongXie JianhuiDai WeiboSu ZirenLiu YuhongLi Yucui - Mitochondrial dysfunction and immune cell metabolic reprogramming are central mechanisms driving the pathogenesis and progression of multiple sclerosis (MS). Fingolimod (FTY720), a sphingosine-1-phosphate analog widely used in MS, limits lymphocyte egress from lymphoid organs; however, its effects on mitochondrial function and immunometabolic pathways remain incompletely understood. We evaluated mitochondrial bioenergetics and metabolic reprogramming in lymphocytes from healthy controls incubated with FTY720 and from MS patients treated with fingolimod, compared with healthy controls and patients receiving interferon-beta or glatiramer acetate. Mitochondrial respiration and glycolytic activity were assessed by extracellular flux analysis under basal conditions and following phytohaemagglutinin (PHA) stimulation, while mitochondrial parameters and metabolic markers were analyzed by flow cytometry and immunoblotting. Fingolimod exhibited a blunted metabolic response to PHA in lymphocytes from acutely-treated controls and patients receiving chronic therapy. In both unstimulated and PHA-stimulated conditions, acute incubation with FTY720 in control lymphocytes displayed decreased basal, maximal, and ATP-linked respiration; and basal and maximal glycolytic activity that resulted in reduced glycolytic reserve. In lymphocytes from in vitro acutely exposed controls and from chronically treated MS patients, fingolimod treatment was associated with decreased mitochondrial mass and membrane potential after PHA-stimulation, with reduced expression of lactate transporters (MCT1 and MCT4). FTY720-treatment in control lymphocytes was associated to lower expression of ETC complex proteins and of those involved in mitochondrial dynamics, and increased ROS and PFKFB3 levels under basal and stimulated conditions. These findings suggest that mitochondrial metabolism of lymphocytes is a potential component of fingolimod activity, promoting an altered bioenergetic state. - Source: PubMed
Publication date: 2026/08/08
González-Jiménez AdelaLópez-Cotarelo PilarMoreno-Jerez AlbaVela-Artiza JordinaMena-Plaza EstelaAladro YolandaPilo BelénOreja-Guevara CeliaGómez-Estévez IreneLópez-Pastor Andrea RGómez-Delgado IreneUrcelay Elena - Chronic wound healing disorders remain a significant clinical challenge, largely due to the limited effectiveness of conventional therapeutic strategies. Emerging evidence suggests that engineered exosomes represent a promising cell-free therapeutic approach. This study aimed to elucidate the mechanisms by which fibroblast growth factor 21 (FGF21)-modified adipose-derived mesenchymal stem cell (ADSC) exosomes promote wound healing. - Source: PubMed
Publication date: 2026/08/04
Chen KeweiChen XiaoyuWen ChenyiChen WanyingLiao ZijinChen YanmingLi Liqun