Ask about this productRelated genes to: TXNIP Blocking Peptide
- Gene:
- TXNIP NIH gene
- Name:
- thioredoxin interacting protein
- Previous symbol:
- -
- Synonyms:
- VDUP1, EST01027, HHCPA78, THIF, ARRDC6
- Chromosome:
- 1q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-12
- Date modifiied:
- 2016-10-05
Related products to: TXNIP Blocking Peptide
Related articles to: TXNIP Blocking Peptide
- This study developed a prognostic model for hepatocellular carcinoma (HCC) based on cancer stem cell (CSC)-related modules identified by high-dimensional WGCNA (hdWGCNA). - Source: PubMed
Publication date: 2026/06/22
Yin XielingZhou YuanChen ShiMa ChunyangWu HongfeiCao HuiShi WeiLiang Chi - NBO therapy has demonstrated a neuroprotective effect on ischemic stroke. This study investigated the role of HIF-1α in regulating SG formation and NLRP3 inflammasome activation following I/R injury in NBO-induced neuroprotection. - Source: PubMed
Publication date: 2026/06/19
Guo SichaoCheng ZheAl Tekreeti AbdullahLi FengwuDing YuchuanGeng Xiaokun - Many studies have indicated that epigenetic mechanisms, particularly DNA methylation, play an important role in regulating genes involved in glucose and lipid metabolism, oxidative stress, and energy homeostasis. Among these, TXNIP and ADRB3 are key metabolic regulators linked to insulin signaling, adipose tissue function, and energy expenditure. This study aimed to evaluate promoter methylation levels of TXNIP and ADRB3 in individuals with metabolic syndrome compared with healthy controls and to investigate their associations with clinical and biochemical parameters. - Source: PubMed
Publication date: 2026/06/19
Dizghandi Saeed EsmaeiliMostafapour SaharKhodabandehloo FatemehAlani BehrangSaremi LeilaKenarangi TaiebeMosallaei MeysamRezvankhah Boshra - Chemotherapy-induced cardiotoxicity is a significant difficulty in chemotherapy, contributing to long-term morbidity and reduced quality of life among cancer survivors. The NLRP3 inflammasome is a crucial molecular association between chemotherapeutic stress and inflammatory cardiomyocyte death, despite the fact that oxidative stress, mitochondrial dysfunction, calcium imbalance, and endothelial injury are well-known factors. NLRP3 activation increases myocardial inflammation and structural damage by stimulating Gasdermin D-dependent pyroptosis and caspase-1-mediated upregulation of IL-1β and IL-18. Another important upstream process that promotes NLRP3 activation during chemotherapy exposure is mitochondrial ROS-induced dissociation of TXNIP. Anthracyclines, antimetabolites, alkylating agents, platinum compounds, and microtubule inhibitors are just a few of the chemotherapeutic classes in which NLRP3 is involved. This review integrates current knowledge of NLRP3 structure, priming and activation pathways, and downstream signalling. This broader perspective illustrates the wider impact of inflammasome-mediated pathophysiology in chemotherapy-induced cardiac failure and goes beyond traditional doxorubicin-centered treatments. The review also provides an overview of the therapeutic landscape of selective NLRP3 inhibition, including natural modulators such as oridonin, curcumin, resveratrol, honokiol, and flavonoids, as well as synthetic inhibitors such as MCC950, CY-09, OLT1177 (dapansutrile), and tranilast. Synthetic molecules exhibit strong target specificity by suppressing NACHT ATPase activity, preventing ASC oligomerization, or inhibiting NEK7-dependent assembly, whereas natural compounds provide broader antioxidant and anti-inflammatory actions with favourable safety. Emerging evidence suggests synergistic benefits when NLRP3 inhibition is paired with antioxidants or established cardioprotective agents. Despite encouraging preclinical findings, translational challenges remain, including long-term safety assessment. Modulation of NLRP3 inflammasome activation has emerged as a potential intervention to limit chemotherapy-induced cardiac injury and dysfunction in cardio-oncology. - Source: PubMed
Publication date: 2026/06/18
Dhondsekar DipilMandlik SatishMandlik Deepa - The senescence of lung epithelial cells impairs self-repair and exacerbates lung damage in idiopathic pulmonary fibrosis. The potential of natural phytochemicals to reverse premature senescence warrants investigation. Information regarding the independent multifaceted effect of quercetin and artemisinin on epithelial senescence has not been delineated yet. The present investigation aimed to comprehend their attributes on HO-induced hallmark of premature senescence via controlling the vicious circle of oxidative-inflammatory stress, impaired cell proliferation, apoptosis, DNA damage, and inflammatory senescence cascades. An in vitro model of HO-exposed BEAS-2B cells was used to explore senescence using microscopy, qRT-PCR, immunoblotting, flow cytometry, and NMR· HO (100 µM) treatment induced cellular senescence-associated features without significant cytotoxicity, as evidenced by enhanced SA-β-galactosidase activity, irreversible irregular enlargement, shrinking, and flattened cell appearance, which was reversed by quercetin and artemisinin at varying degree. Results revealed that quercetin and artemisinin restored disrupted mitochondrial function in senescent cells, as evidenced by reduced MMP, GLS, ARRDC4, TXNIP, creatine, and increased NRF-2, HO-1, NQO-1, Sirt-1/5, and glycine levels. Furthermore, quercetin and artemisinin promoted proliferative ability, DNA repair, S-phase cell cycle transition, apoptosis, and suppressed SASP, as evidenced by enhanced Ki67 expression, annexin-V-positive cells, and diminished expression of interleukins, COX-2, MMPs, and the Atm/p53/p16/p21/Bcl-2 axis. Subsequently, activation of NOD-1, Stat-1, NF-κB, ERK1/2, p38, and JNK was decisively thwarted by quercetin and artemisinin. Intriguingly, Lamin B1 restoration and ROS inhibition were only noticed in quercetin, indicating both are effective in halting senescence through an alternative pathway. Overall, the present investigation emphasizes that quercetin and artemisinin exhibit both senolytic and senomorphic properties and could be valuable senotherapeutics for stress-induced premature senescence. - Source: PubMed
Publication date: 2026/06/08
Karadagatla SumanPadhy Hara PrasadSharma Anamika