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Our study showed the pivotal role of RORalpha as an inhibitor of the thermogenic program in white adipose tissue
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We have identified RORalpha as a regulator of Treg genes responsible for suppressing allergic skin inflammation and also documented higher expression of RORalpha in skin-resident Tregs than in peripheral blood circulating Tregs in humans, suggesting that RORalpha and the TL1A-DR3 circuit could be therapeutically targeted in atopic dermatitis.
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These findings demonstrated for the first time that nuclear receptor RORalpha deficiency aggravated HFD-induced myocardial dysfunction at least in part by impairing mitochondrial biogenesis in association with disrupting AMPK-PGC1alpha signaling.
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RORalpha/gamma controls circadian expression of Insig2, which keeps feeding-induced SREBP1c activation under check
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RORalpha induces KLF4 mediated Kupffer cells polarization and protects against NASH.
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RORalpha/gamma are important therapeutic targets for cutaneous inflammation; RORa and RORg have roles in inflammation in mouse models of atopic dermatitis and acute irritant dermititis
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Data demonstrated that the circadian rhythm of testosterone synthesis in TM3 cells was disturbed following Fen treatment as evidenced by changes in the circadian rhythmicity of core clock genes (Bmal1, Rev-erbalpha, Roralpha).
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RORalpha inhibits PPARgamma-mediated transcriptional activity by interacting with HDAC3 and competing for the promoters of lipogenic genes.
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The expression RORalpha is significantly elevated under hypoxic conditions in keratinocytes in an HIF-1alpha dependent manner.
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that retinoic acid receptor-related orphan receptor alpha is a novel transcriptional regulator of SEMA3E-mediated neurovascular coupling in pathological retinal angiogenesis
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The deficiency of LXRalpha decreased glucose uptake after MI, resulting in a metabolic shift that suppressed glucose metabolism, which was in association with adverse cardiac remodeling.
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Data suggest that inflammatory response in macrophages, white adipocytes, and white adipose tissue in obese mice, includes up-regulation of expression of Rora; in adipose tissue, overexpression of Rora or treatment with Rora agonist enhances expression of cytokines, promotes macrophage infiltration, up-regulates expression of genes involved in ER stress response, and enhances signaling seen in unfolded protein response.
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these findings reveal that RORalpha regulates macrophage M2 polarization via activation of AMPKalpha
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RORalpha-dependent type 2 innate lymphoid cells are required and sufficient for type 2 cytokine expression and mucous metaplasia in immature mice.
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pharmacological activation of RORalpha by melatonin and SR1078 (a synthetic agonist) showed beneficial effects against diabetic cardiomyopathy, while the RORalpha inhibitor SR3335 significantly exacerbated cardiac impairments in diabetic mice.
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study provides the first direct evidence that the nuclear melatonin receptor RORalpha is a novel endogenous protective receptor against MI/R injury and an important mediator of melatonin-exerted cardioprotection; melatonin-RORalpha axis signaling thus appears important in protection against ischemic heart injury.
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RORalpha regulates pathologic retinal angiogenesis by modulating SOCS3-dependent inflammation
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This study showed that spontaneous Rora mutations causing cerebellar pathology are impaired in motor functions during the neonatal period.
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the inhibition of NF-kappaB by melatonin, but not that of NLRP3, was blunted in RORalpha (sg/sg) mice, indicating that functional RORalpha transcription factor is necessary for the initiation of the innate immune response against inflammation.
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Identify RORalpha as being essential to drive inflammation in experimental epidermolysis bullosa acquisita.
