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Last update 08 May 2025

ERRα

Last update 08 May 2025

Basic Info

Synonyms

ERR-alpha, ERR1, ERRa

+ [9]

Introduction

Binds to an ERR-alpha response element (ERRE) containing a single consensus half-site, 5'-TNAAGGTCA-3'. Can bind to the medium-chain acyl coenzyme A dehydrogenase (MCAD) response element NRRE-1 and may act as an important regulator of MCAD promoter. Binds to the C1 region of the lactoferrin gene promoter. Requires dimerization and the coactivator, PGC-1A, for full activity. The ERRalpha/PGC1alpha complex is a regulator of energy metabolism. Induces the expression of PERM1 in the skeletal muscle.

Drugs associated with ERRα

DS20362725

Target

ERRα

Mechanism

ERRα agonists

Active Org.

Daiichi Sankyo Co., Ltd.

Originator Org.

Daiichi Sankyo, Inc.

Active Indication-

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

XCT-790

Target

ERRα

Mechanism

ERRα antagonists

Active Org.

X-Ceptor Therapeutics, Inc. [+2]

Originator Org.

San Francisco Conservatory of Music [+1]

Active Indication

Acute Myeloid Leukemia [+3]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

DS45500853

Target

ERRα

Mechanism

ERRα agonists

Active Org.

Daiichi Sankyo Co., Ltd.

Originator Org.

Daiichi Sankyo Co., Ltd.

Active Indication-

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with ERRα

100 Translational Medicine associated with ERRα

0 Patents (Medical) associated with ERRα

945

Literatures (Medical) associated with ERRα

01 Aug 2025·Gene

miR-125b-5p regulates FFA-induced hepatic steatosis in L02 cells by targeting estrogen-related receptor alpha

Article

Author: Ma, Yanhua ; Duan, Qianchen ; Gao, Fen ; Yu, Chun

BACKGROUND & AIMSNAFLD is a global and complex liver disease caused by multiple factors. Intrahepatocellular steatosis is the primary prerequisite for the occurrence and development of NAFLD. It has been shown that miR-125b-5p is highly correlated with NAFLD, and ESRRA is a factor that regulates lipid metabolism. The purpose of our study is to investigate whether miR-125b-5p regulates FFA-induced steatosis in L02 cells by targeting ESRRA.APPROACHES AND RESULTSEstrogen-related receptor alpha (ESRRA) was identified as a direct target of miR-125b-5p through database prediction and a dual-luciferase reporter gene assay. L02 cells were induced with free fatty acids (OA:PA, 2:1) at concentrations of 0.3 mM, 0.6 mM, 0.9 mM, 1.2 mM and 1.5 mM for 24 h, 48 h and 72 h, respectively. The degree of hepatocyte steatosis and triglyceride content were separately manifested by oil red O staining and colorimetric method. Cell viability per group was detected by CCK-8 assay. Eventually, 0.9 mM and 24 h were screened out as the optimal concentration and time for establishing the in-vitro model of hepatic steatosis. Followingly, miR-125b-5p and ESRRA were knocked down by transient transfection. We monitored the expressions of lipid metabolism factors SREBP-1c, ACC1 and FAS. The data showed that knockdown of ESRRA led to down-regulation of the expressions of SREBP-1, ACC1 and FAS. Meanwhile, knockdown of ESRRA and miR-125b-5p resulted that the expressions of ESRRA, SREBP-1, ACC1 and FAS rebounded.CONCLUSIONSMiR-125b-5p down-regulates the expressions of lipid metabolism-related factors by negatively regulating ESRRA, thereby improving hepatic steatosis.

01 Jul 2025·Free Radical Biology and Medicine

Dapagliflozin attenuates diabetes-induced podocyte lipotoxicity via ERRα-Mediated lipid metabolism

Article

Author: Fan, Yanqin ; Yang, Qian ; Hu, Jijia ; Peng, Zhuan ; Hu, Hongtu ; Wang, Juan

Diabetic kidney disease (DKD) is a major complication of diabetes mellitus, characterized by podocyte injury and lipid accumulation, which contribute to high morbidity and mortality. Current treatments primarily alleviate symptoms, underscoring the need for targeted therapies to address the underlying mechanisms of DKD progression. This study explores the protective effects of dapagliflozin (DAPA), a selective sodium-glucose cotransporter 2 (SGLT2) inhibitor, on podocyte lipotoxicity and its regulatory role in the estrogen-related receptor alpha (ERRα)-acyl-CoA oxidase 1 (ACOX1) axis. Using db/db mice and streptozotocin-induced DKD models, we demonstrate that DAPA significantly reduces the urinary albumin-to-creatinine ratio (ACR) and improves renal pathology by alleviating glomerular hypertrophy, mesangial matrix expansion, and podocyte foot process effacement. DAPA also decreases triglyceride and free fatty acid accumulation in glomeruli, as evidenced by Oil Red O and BODIPY staining. Mechanistically, DAPA upregulates ERRα and ACOX1 expression in podocytes, enhancing fatty acid oxidation (FAO) and mitigating lipidtoxicity. Loss of ERRα exacerbates lipid-induced podocyte injury, while ERRα overexpression confers protective effects. These findings highlight DAPA's renoprotective effects via modulation of the ERRα-ACOX1 axis, suggesting that targeting ERRα could be a promising therapeutic strategy for DKD.

01 Apr 2025·Journal of Cachexia, Sarcopenia and Muscle

Oestrogen Receptor Alpha in Myocyte Maintains Muscle Regeneration in Duchenne Muscular Dystrophy

Article

Author: Fan, Shusheng ; Tong, Haowei ; Li, Sijia ; Zhao, Lei ; Yu, Qinwei ; Wang, Huna ; Xu, Dengqiu ; Li, Xihua ; Zhang, Luyong ; Guo, Guangyao ; Huang, Xiaofei ; Jiang, Zhenzhou ; Hu, Wanting

ABSTRACTBackgroundOestrogen receptor alpha (ERα) plays an important role in maintaining mitochondrial function and regulating metabolism in skeletal muscle. However, its alterations and potential mechanisms in Duchenne muscular dystrophy (DMD) remain incompletely understood. In this study, we demonstrated the protective role of ERα in myocyte for skeletal muscle regeneration in mdx mice and explored the therapeutic effects of oestrogen receptor modulators on DMD.MethodsDMD patients' biopsies were obtained for histological analysis to explore the expression of ERα. The phenotype of muscle was analysed by histology and molecular biology. The therapeutical effect of different oestrogen receptor modulators was examined in mdx mice treated with fulvestrant (FVT, 20 mg/kg once a week) or oestradiol (E2, 1 mg/kg per day) for 4 weeks. The protective effect of ERα was performed on mdx mice after conditional knockout of ERα in skeletal muscle (ERαmKOmdx mice). Evidence of activation of ERα/oestrogen‐related receptor alpha (ERRα)/myogenic differentiation 1 (MyoD) signalling pathway was inspected in the primary myoblasts isolated from mice, and C2C12 cells received intervention with E2/FVT/Esr1‐siRNA/Esrra overexpression plasmid.ResultsThe ERα expression was increased in DMD patients' triceps (p < 0.05) and mdx mice muscles (p < 0.05). FVT reduced ERα levels in the mdx mice muscles (p < 0.01) but had no significant effect on skeletal muscle regeneration on mdx mice. Compared with mdx mice, E2 reduced the levels of creatine kinase (CK) and lactic dehydrogenase (LDH) (p < 0.001) in serum, enhanced skeletal muscle function, alleviated skeletal muscle atrophy and fibre loss and upregulated the expression of ERα in GAS (p < 0.001) and TA (p < 0.05). The myogenic factors such as myosin heavy chain (MyHC, p < 0.001), myogenin (MyoG, p < 0.05), MyoD (p < 0.05) and ERRα (p < 0.001) were increased in mdx mice GAS with E2. But E2 had no effect on ERαmKOmdx mice. The primary myoblasts and C2C12 were treated with E2 displayed an increased‐on myocyte fusion index (p < 0.05), ERα MyoD and ERRα expressions (p < 0.05). The myocytes' fusion index (p < 0.05) and ERα, MyoD and ERRα expression (p < 0.05) were decreased in si‐Esr1‐transfected C2C12 cells and increased in OE‐Esrra‐transfected C2C12 cells.ConclusionWe demonstrated that ERα in myocyte exerted a protective effect on skeletal muscle regeneration in DMD patients and mdx mice through the ERα‐ERRα‐MyoD pathway, which has potential implications for DMD therapy strategies.

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ERRα

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