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Metformin protects against diclofenac-induced toxicity in primary rat hepatocytes by preserving mitochondrial integrity via a pathway involving EPAC.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Mora FAA, Musheshe N, Arroyave Ospina JC, Geng Y, Soto JM, Rodrigo JA, Alieva T, Buist-Homan M, Lezoualc'h F, Cheng X, Schmidt M, Moshage H.
PMID: 34464747
Biomed Pharmacother. 2021 Nov;143:112072. doi: 10.1016/j.biopha.2021.112072. Epub 2021 Aug 28.

BACKGROUND AND PURPOSE: It has been shown that the antidiabetic drug metformin protects hepatocytes against toxicity by various stressors. Chronic or excessive consumption of diclofenac (DF) - a pain-relieving drug, leads to drug-induced liver injury via a mechanism involving...

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Mora FAA, Musheshe N, Arroyave Ospina JC, et al. Metformin protects against diclofenac-induced toxicity in primary rat hepatocytes by preserving mitochondrial integrity via a pathway involving EPAC. Biomed Pharmacother. 2021;143:112072doi: 10.1016/j.biopha.2021.112072.
Mora, F. A. A., Musheshe, N., Arroyave Ospina, J. C., Geng, Y., Soto, J. M., Rodrigo, J. A., Alieva, T., Buist-Homan, M., Lezoualc'h, F., Cheng, X., Schmidt, M., & Moshage, H. (2021). Metformin protects against diclofenac-induced toxicity in primary rat hepatocytes by preserving mitochondrial integrity via a pathway involving EPAC. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 143112072. https://doi.org/10.1016/j.biopha.2021.112072
Mora, Fabio Alejandro Aguilar, et al. "Metformin protects against diclofenac-induced toxicity in primary rat hepatocytes by preserving mitochondrial integrity via a pathway involving EPAC." Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie vol. 143 (2021): 112072. doi: https://doi.org/10.1016/j.biopha.2021.112072
Mora FAA, Musheshe N, Arroyave Ospina JC, Geng Y, Soto JM, Rodrigo JA, Alieva T, Buist-Homan M, Lezoualc'h F, Cheng X, Schmidt M, Moshage H. Metformin protects against diclofenac-induced toxicity in primary rat hepatocytes by preserving mitochondrial integrity via a pathway involving EPAC. Biomed Pharmacother. 2021 Nov;143:112072. doi: 10.1016/j.biopha.2021.112072. Epub 2021 Aug 28. PMID: 34464747.
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Cyclic AMP-binding protein Epac1 acts as a metabolic sensor to promote cardiomyocyte lipotoxicity.

Cell death & disease

Laudette M, Sainte-Marie Y, Cousin G, Bergonnier D, Belhabib I, Brun S, Formoso K, Laib L, Tortosa F, Bergoglio C, Marcheix B, Borén J, Lairez O, Fauconnier J, Lucas A, Mialet-Perez J, Moro C, Lezoualc'h F.
PMID: 34471096
Cell Death Dis. 2021 Sep 01;12(9):824. doi: 10.1038/s41419-021-04113-9.

Cyclic adenosine monophosphate (cAMP) is a master regulator of mitochondrial metabolism but its precise mechanism of action yet remains unclear. Here, we found that a dietary saturated fatty acid (FA), palmitate increased intracellular cAMP synthesis through the palmitoylation of...

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Laudette M, Sainte-Marie Y, Cousin G, et al. Cyclic AMP-binding protein Epac1 acts as a metabolic sensor to promote cardiomyocyte lipotoxicity. Cell Death Dis. 2021;12(9):824doi: 10.1038/s41419-021-04113-9.
Laudette, M., Sainte-Marie, Y., Cousin, G., Bergonnier, D., Belhabib, I., Brun, S., Formoso, K., Laib, L., Tortosa, F., Bergoglio, C., Marcheix, B., Borén, J., Lairez, O., Fauconnier, J., Lucas, A., Mialet-Perez, J., Moro, C., & Lezoualc'h, F. (2021). Cyclic AMP-binding protein Epac1 acts as a metabolic sensor to promote cardiomyocyte lipotoxicity. Cell death & disease, 12(9), 824. https://doi.org/10.1038/s41419-021-04113-9
Laudette, Marion, et al. "Cyclic AMP-binding protein Epac1 acts as a metabolic sensor to promote cardiomyocyte lipotoxicity." Cell death & disease vol. 12,9 (2021): 824. doi: https://doi.org/10.1038/s41419-021-04113-9
Laudette M, Sainte-Marie Y, Cousin G, Bergonnier D, Belhabib I, Brun S, Formoso K, Laib L, Tortosa F, Bergoglio C, Marcheix B, Borén J, Lairez O, Fauconnier J, Lucas A, Mialet-Perez J, Moro C, Lezoualc'h F. Cyclic AMP-binding protein Epac1 acts as a metabolic sensor to promote cardiomyocyte lipotoxicity. Cell Death Dis. 2021 Sep 01;12(9):824. doi: 10.1038/s41419-021-04113-9. PMID: 34471096; PMCID: PMC8410846.
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Targeting epigenetic mechanisms as an emerging therapeutic strategy in pulmonary hypertension disease.

Vascular biology (Bristol, England)

Bisserier M, Janostiak R, Lezoualc'h F, Hadri L.
PMID: 32161845
Vasc Biol. 2020 Jan;2(1):R17-R34. doi: 10.1530/vb-19-0030. Epub 2020 Jan 09.

Pulmonary arterial hypertension (PAH) is a multifactorial cardiopulmonary disease characterized by an elevation of pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR), which can lead to right ventricular (RV) failure, multi-organ dysfunction, and ultimately to premature death. Despite...

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Bisserier M, Janostiak R, Lezoualc'h F, et al. Targeting epigenetic mechanisms as an emerging therapeutic strategy in pulmonary hypertension disease. Vasc Biol. 2020;2(1):R17-R34doi: 10.1530/vb-19-0030.
Bisserier, M., Janostiak, R., Lezoualc'h, F., & Hadri, L. (2020). Targeting epigenetic mechanisms as an emerging therapeutic strategy in pulmonary hypertension disease. Vascular biology (Bristol, England), 2(1), R17-R34. https://doi.org/10.1530/vb-19-0030
Bisserier, Malik, et al. "Targeting epigenetic mechanisms as an emerging therapeutic strategy in pulmonary hypertension disease." Vascular biology (Bristol, England) vol. 2,1 (2020): R17-R34. doi: https://doi.org/10.1530/vb-19-0030
Bisserier M, Janostiak R, Lezoualc'h F, Hadri L. Targeting epigenetic mechanisms as an emerging therapeutic strategy in pulmonary hypertension disease. Vasc Biol. 2020 Jan;2(1):R17-R34. doi: 10.1530/vb-19-0030. Epub 2020 Jan 09. PMID: 32161845; PMCID: PMC7065685.
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Estrogens with an intact phenolic group prevent death of neuronal cells following glutathione depletion.

Restorative neurology and neuroscience

Behl C, Lezoualc'h F.
PMID: 12671307
Restor Neurol Neurosci. 1998 Jun;12(2):127-34.

Oxidative stress-induced neurodegeneration has been implicated in a variety of neuropsychiatric disorders including Alzheimer's disease (AD). Therefore, neuroprotection is of central interest in basic and preclinical neuroscience. Recently, we reported that the AD-associated amyliod beta protein can induce neuronal...

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Behl C, Lezoualc'h F. Estrogens with an intact phenolic group prevent death of neuronal cells following glutathione depletion. Restor Neurol Neurosci. 1998;12(2):127-34
Behl, C., & Lezoualc'h, F. (1998). Estrogens with an intact phenolic group prevent death of neuronal cells following glutathione depletion. Restorative neurology and neuroscience, 12(2), 127-34.
Behl, C, and Lezoualc'h, F. "Estrogens with an intact phenolic group prevent death of neuronal cells following glutathione depletion." Restorative neurology and neuroscience vol. 12,2 (1998): 127-34.
Behl C, Lezoualc'h F. Estrogens with an intact phenolic group prevent death of neuronal cells following glutathione depletion. Restor Neurol Neurosci. 1998 Jun;12(2):127-34. PMID: 12671307.
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Epac Function and cAMP Scaffolds in the Heart and Lung.

Journal of cardiovascular development and disease

Laudette M, Zuo H, Lezoualc'h F, Schmidt M.
PMID: 29401660
J Cardiovasc Dev Dis. 2018 Feb 03;5(1). doi: 10.3390/jcdd5010009.

Evidence collected over the last ten years indicates that Epac and cAMP scaffold proteins play a critical role in integrating and transducing multiple signaling pathways at the basis of cardiac and lung physiopathology. Some of the deleterious effects of...

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Laudette M, Zuo H, Lezoualc'h F, et al. Epac Function and cAMP Scaffolds in the Heart and Lung. J Cardiovasc Dev Dis. 2018;5(1)doi: 10.3390/jcdd5010009.
Laudette, M., Zuo, H., Lezoualc'h, F., & Schmidt, M. (2018). Epac Function and cAMP Scaffolds in the Heart and Lung. Journal of cardiovascular development and disease, 5(1), . https://doi.org/10.3390/jcdd5010009
Laudette, Marion, et al. "Epac Function and cAMP Scaffolds in the Heart and Lung." Journal of cardiovascular development and disease vol. 5,1 (2018). doi: https://doi.org/10.3390/jcdd5010009
Laudette M, Zuo H, Lezoualc'h F, Schmidt M. Epac Function and cAMP Scaffolds in the Heart and Lung. J Cardiovasc Dev Dis. 2018 Feb 03;5(1). doi: 10.3390/jcdd5010009. PMID: 29401660; PMCID: PMC5872357.
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Showing 1 to 5 of 5 entries