Ask about this productRelated genes to: AGTR1 antibody
- Gene:
- AGTR1 NIH gene
- Name:
- angiotensin II receptor type 1
- Previous symbol:
- AGTR1B
- Synonyms:
- AT1, AT2R1, AGTR1A, AT2R1A, HAT1R, AG2S, AT2R1B, AT1B
- Chromosome:
- 3q24
- Locus Type:
- gene with protein product
- Date approved:
- 1992-08-25
- Date modifiied:
- 2017-07-07
Related products to: AGTR1 antibody
Related articles to: AGTR1 antibody
- Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, with limited therapeutic options. Radiotherapy (RT) is a cornerstone of TNBC treatment; however, preclinical studies suggest that RT may both stimulate and suppress immune responses within the tumor microenvironment (TME). While RT can enhance immune responses, it may also induce an immunosuppressive TME, contributing to radioresistance. The renin-angiotensin system (RAS) is also involved in the immunosuppressive TME and tumor radioresistance. Previous research showed blocker of angiotensin II receptor (AGTR1), losartan, as a RAS inhibitor, could alleviate hypoxia, thereby enhancing RT efficacy. Our study shows that high levels of AGTR1 may confer a poor prognosis and radioresistance in TNBC, and innovatively demonstrates losartan could enhance the radiosensitivity of TNBC in an immune dependent way. Furthermore, we found losartan could inhibit tumor-associated macrophages (TAMs) polarizing towards M2 phenotype, impedes the immunosuppressive function of myeloid-derived suppressive cells (MDSCs) induced by RT, and ultimately up-regulates the number and function of tumor-infiltrating CD8 T lymphocytes. Besides, RNA-seq data reveals losartan impedes JAK2/STAT1 signaling activation upon irradiation, suppresses the interferon-related DNA damage resistant signature (IRDS) expression and diminishes the immune suppressive factors PD-L1 and IDO induced by irradiation in TNBC cells. Collectively, in our study, we investigate the role of losartan in radiosensitization and demonstrate losartan could reverse the immunosuppressive TME induced by RT in TNBC, which suggests that losartan combined with RT may represent a promising strategy for the treatment of TNBC. - Source: PubMed
Publication date: 2026/05/07
Wang XuLiu CuiweiXia ZihanHu TingLi YutingHan DanSong YunjieMa YuxiZhao Yanxia - Dextromethorphan (DEX) is a commonly used antitussive agent and N-methyl-D-aspartate (NMDA) receptor antagonist that has been reported to cause different organ impairments. The current investigation was conducted to systematically assess the doses dependent effects of DEX on kidneys. Thirty-two Sprague Dawley rats were categorized into control group, DEX (20 mg/kg), DEX (40 mg/kg) and DEX (80 mg/kg) administered group. DEX exposure led to upregulation of Renin, angiotensin converting enzyme (ACE), and angiotensin II receptor type I (AGTR1) while downregulated the expression of angiotensin II receptor type II (AGTR2), organic anion transporter 1 (Oat1), organic anion transporter 3 (Oat3), organic cation transporter 3 (Oct2), and multidrug resistance-associated protein 2 (Mrp2) in dose-dependent manners. Moreover, DEX intoxication suppressed the activities of catalase (CAT), glutathione peroxidase (GPx), heme-oxygenase-1 (HO-1), superoxide dismutase (SOD), and glutathione reductase (GSR) while promoting the concentrations of reactive oxygen species (ROS) and malondialdehyde (MDA). Similarly, DEX administration caused significant deterioration of renal function as indicated by significant elevations of serum urea, uric acid, blood urea nitrogen, with a marked reduction in the concentration of creatinine clearance. Furthermore, a notable upsurge was observed in the levels of kidney injury molecule-1 (KIM-1), Neutrophilic gelatinase-associated lipocalin (NGAL), N-acetyl glucosamine (NAG), Cystatin-C, Osteopontin, and Endothelin-1 after DEX exposure. Mechanistically, DEX significantly altered the apoptotic balance, elevating the levels of Bcl-2-associated protein X (Bax), cystine aspartic acid protease-3 (caspase-3), and cystine aspartic acid protease-9 (caspase-9) while reducing the levels of B-cell lymphoma-2 (Bcl-2). In parallel, DEX evoked a strong inflammatory response, which was characterized by increased concentrations of nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-1 beta (IL-1β) and cyclooxygenase-2 (COX-2). Histopathological evaluation supported these data, as it showed progressive dose-dependent renal damage from tubular degeneration to extensive glomerular collapse, interstitial edema, and inflammation. Collectively, these findings proved that sub-chronic exposure to DEX exerts a marked nephrotoxic effect via coordinated disruption of renal function, inflammatory homeostasis and apoptotic signaling. This study provides new mechanistic insights into DEX-induced renal impairments and emphasizes the importance of a strong regulatory policy. - Source: PubMed
Publication date: 2026/05/01
Alissa MohammedAlghamdi Suad ABinshaya Abdulkarim SAlqarni Adel MSafhi Awaji YSabei Fahad YAlbati Amal AAbalkhail Adil - Sheep feeding systems strongly influence meat quality, animal health, and production efficiency. Grazing improves fatty acid composition and sustainability but limits productivity, whereas concentrate feeding enhances efficiency but may induce oxidative stress. Vitamin E (VE), a key antioxidant, may mitigate these effects; however, systematic multi-tissue molecular evidence remains limited. - Source: PubMed
Publication date: 2026/04/24
Xu HaoranShi Jie - A significant residual risk of myocardial infarction (MI) persists in hypertensive patients treated with angiotensin receptor blockers (ARBs). Conventional risk models often fail to capture the complex, nonlinear interactions among clinical phenotypes, comorbidities, and pharmacogenetic factors. - Source: PubMed
Publication date: 2026/04/01
Chu QiZhang SiwenZhang HanKong LingjunWang ShashaDou Yaling - Antihypertensive therapy is pivotal in preventing cardiovascular events, yet treatment efficacy varies significantly among individuals due to genetic polymorphisms.This study aimed to investigate the association between specific antihypertensive drug-related gene polymorphisms, the use of corresponding sensitive drugs, and the risks of stroke and coronary heart disease (CHD) in a community-based hypertensive population. A cross-sectional study was conducted among 29,662 hypertensive patients from primary care centers in Changsha County, China. Seven gene loci (ACE(I/D), CYP2C9*3,AGTR1(1166 A > C), CYP2D6*10,ADRB1(1165G > C), CYP3A5*3, and NPPA(2238T > C))were genotyped.Patients were stratified into sensitive or non-sensitive genotype groups. Logistic regression and interaction analysis were employed to assess gene-drug interactions on cardiovascular outcomes. The prevalence of stroke and CHD was 2.8% and 19.5%, respectively. Carriers of sensitive genotypes for AGTR1, CYP2D6*10, and ADRB1 taking sensitive drugs exhibited a significantly lower risk of stroke (ORs: 0.39, 0.67, 0.68; all P < 0.01). Similarly, sensitive genotype carriers for CYP2D6*10, CYP3A5*3, and NPPA taking sensitive drugs had a reduced risk of CHD (ORs: 0.92, 0.88, 0.53; all P < 0.05). A significant additive interaction was identified between AGTR1(1166 A > C) and sensitive drug use on CHD risk (AP = 0.08). Pharmacogenomics-guided antihypertensive therapy is associated with a reduced risk of stroke and CHD in hypertensive patients. The interaction between AGTR1(1166 A > C) genotype and drug use underscores the potential of personalized medicine in optimizing cardiovascular disease prevention strategies in primary care. - Source: PubMed
Publication date: 2026/04/12
Li ZetongLiu HuixiaChen MengshiDeng JingMa ZiyuHuang GeLi ChengSu MengZhong Hua