Regular ArticleAngiotensin II Induces Nuclear Factor- κ B Activation in Cultured Neonatal Rat Cardiomyocytes Through Protein Kinase C Signaling Pathway
References (25)
- et al.
Signaling pathways in cardiac myocyte hypertrophy
J Mol Cell Cardiol
(1997) - et al.
Multiple signals converging on NF- κ B
Curr Opinion Cell Biol
(1999) - et al.
Signal transduction through NF- κ
Immunol Today
(1998) - et al.
Terminally differentiated neonatal rat myocardial cells proliferate and maintain specific functions following expression of SV 40 large T antigen
J Biol Chem
(1988) A rapid and sensitive method for quantification of microgram quantities of protein utilizing the principle of protein-dye binding
Anal Biochem
(1976)- et al.
Eukaryotic gene transcription with purified components
Methods Enzymol
(1983) - et al.
Angiotensin II activates the proinflammatory transcription nuclear factor- κ B in human monocytes
Biochem Biophysic Res Comm
(1999) - et al.
Cardiac hypertrophy: mechanical, neural, and endocrine dependence
Circulation
(1991) - et al.
Cellular mechanism of cardiac hypertrophy
Br Heart J
(1995) - et al.
Mechanical stretch induces enhanced expression of angiotensin II receptor subtypes in neonatal rat cardiac myocytes
Circ Res
(1996)
Molecular mechanisms of angiotensin II in modulating cardiac function: intracardiac effects and signal transduction pathways
J Mol Cell Cardiol
Molecular characterization of angiotensin II-induced hypertrophy of cardiac myocytes and hyperplasia of cardiac fibroblasts: a critical role of the AT1 receptor subtype
Circ Res
Cited by (98)
Suppression of TGP on myocardial remodeling by regulating the NF-κB pathway
2018, Biomedicine and PharmacotherapyProtective effects of tannic acid on acute doxorubicin-induced cardiotoxicity: Involvement of suppression in oxidative stress, inflammation, and apoptosis
2017, Biomedicine and PharmacotherapyCitation Excerpt :We observed a significant reduction in DOX-induced NF-κB activity involving TA. It has been suggested that inhibition of NF-κB or anti-NF-κB therapy could serve as possible therapeutic targets incardiotoxicity [57]. Growing evidence demonstrates that DOX-induced apoptotic death of cardiomyocytes is the most direct cause of DOX cardiotoxicity [58].
Can heart function lost to disease be regenerated by therapeutic targeting of cardiac scar tissue?
2016, Seminars in Cell and Developmental BiologyCitation Excerpt :Inhibiting the angiotensin II pathway by administration of losartan was reported to decrease interstitial fibrosis, increase CV, and raise GJ conductance in infarcted hearts [185,186]. Losartan mode-of-action is thought to include the deactivation of MMPs [187–189]. Several studies directed at inhibiting specific inflammatory molecules or the conversion of fibroblasts to myofibroblasts have been completed.
The ocular renin-angiotensin system: A therapeutic target for the treatment of ocular disease
2014, Pharmacology and TherapeuticsCitation Excerpt :Remodeling, when inappropriate, can lead to poor wound healing and failure of a surgical procedure such as failure to lower IOP in glaucoma surgery. It is known that Ang II induces gene expression of TGF-β and matrix metalloproteinase (MMP)-9 precursors (Rouet-Benzineb et al., 2000; Boffa et al., 2003) and as noted previously, mast cell chymase can convert Ang I to Ang II (Reilly et al., 1982; Urata et al., 1990). However, chymase can also promote activation of TGF-β and MMP-9 independently of Ang II (Takai et al., 2010).
Preventive effects of fasudil on adriamycin-induced cardiomyopathy: Possible involvement of inhibition of RhoA/ROCK pathway
2011, Food and Chemical ToxicologyProtective effects of angiotensin-converting enzyme I/I and matrix metalloproteinase-3 6A/6A polymorphisms on dilatative pathology within the ascending thoracic aorta
2011, European Journal of Cardio-thoracic Surgery
- f1
Please address all correspondence to: Patricia Rouet-Benzineb, INSERM U 492/Faculté de Médecine, 8, rue du Général Sarrail, 94010 CRETEIL Cedex, France. E-mail: [email protected]