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NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_1.

ABSTRACT: Elucidation of the mechanisms underpinning doxorubicin-induced toxicity in human AC16 cells and the protection afforded by the NRF2 inducer CDDO-Me.

ORGANISM(S): Homo sapiens

PROVIDER: GSE313504 | GEO | 2025/12/12

REPOSITORIES: GEO

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NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_2.

Project description:Sequencing study was performed to elucidate the mechanisms underpinning doxorubicin-induced toxicity in human AC16 cells and the protection afforded by the NRF2 inducer CDDO-Me.

2025-12-12 | GSE313552 | GEO

NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_3.

2025-12-12 | GSE313503 | GEO

NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_3.

Project description:NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_3.

| PRJNA1379665 | ENA

NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_2.

Project description:NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_2.

| PRJNA1380307 | ENA

NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_1.

Project description:NRF2 upregulation by CDDO-Me protects AC16 human cardiomyocytes against doxorubicin-induced toxicity_1.

| PRJNA1379664 | ENA

Expression profiling by array in livers of Nrf2 null mice administered CDDO-IM

Project description:Nrf2 null mice administered CDDO-IM Nrf2 null mice treated with CDDO-IM

2014-02-18 | E-GEOD-55003 | biostudies-arrayexpress

Expression profiling by array in livers of Nrf2 null mice administered CDDO-IM

Project description:Nrf2 null mice administered CDDO-IM

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Comparative gene expression analysis of Nrf2 activators, CDDO-Im, CDDO-Me and dimethyl fumarate (DMF) in VC1 lung cancer cells

Project description:Nrf2 is an important therapeutic target as activation of this pathway detoxifies harmful insults and reduces oxidative stress. However, the role of Nrf2 in cancer biology is controversial. Protection against oxidative stress and inflammation can confer a survival advantage to tumor cells, leading to a poor prognosis, and constitutive activation of Nrf2 has been detected in numerous tumors. In our study, we examined the role of two clinically relevant classes of Nrf2 activators, the synthetic triterpenoids (CDDO-Im and CDDO-Me) and dimethyl fumarate (DMF) in lung cancer. Using microarrays, we attempt to examine whether these Nrf2 activators have an effect on the same subset of Nrf2 genes.

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RNA sequencing of AC16 and AC16-CAR cells

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The NRF2 inducer CDDO-2P-Im provokes a reduction in amyloid beta levels in Alzheimer’s disease model mice

Project description:Alzheimer’s disease (AD) is the most common etiology of dementia. The transcription factor NF-E2-related factor 2 (NRF2) induces the expression of genes encoding phase II detoxification and antioxidant genes. NRF2 is regulated by Kelch-like ECH-associated protein 1 (KEAP1), and the KEAP1-NRF2 system is the key regulatory system involved in cytoprotection. To examine whether pharmacological induction of NRF2 expression alleviates AD phenotypes in vivo, we employed two AD mouse models, i.e., AppNL-G-F/NL-G-F (AppNLGF) and APPV717I::TAUP301L (APP/TAU) mice. As the synthetic oleanane triterpenoid 1-[2-cyano-3,12-dioxooleana-1,9(11-dien-28-oyl)] (CDDO)-4(-pyridin-2-yl)-imidazole (CDDO-2P-Im) exhibits strong NRF2-inducing activity, in this study, we treated AD model mice with CDDO-2P-Im.

2024-09-09 | GSE271154 | GEO

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