Nrf2 deficiency aggravates Angiotensin II-induced cardiac injury by increasing hypertrophy and enhancing IL-6/STAT3-dependent inflammation

Sulforaphane prevents angiotensin II‐induced cardiomyopathy by activation of Nrf2 through epigenetic modification

“…22 The activation of Nrf2 has been shown to suppress oxidative stress-related cardiac hypertrophy, 25,51 while exacerbated by knockdown of Nrf2. 23 Therefore, Nrf2 is widely regarded to be activated under stress, however, our study suggested that the expression and transcription function of Nrf2 was not significantly increased after 2 months of Ang II stimulation (Figure 3). It is possible that the activation of some inhibitory factors or long-term oxidative stress stimulation has impaired Nrf2 function, causing the disappearance of its compensatory protective effect, which will ultimately result in more severe cardiac damage.…”

“…22 It has been determined that Nrf2 is essential to protect against cardiomyopathy induced by Ang II. [23][24][25] The overexpression of Nrf2 inhibits cardiomyopathy and ROS produced by Ang II administration, whereas the absence of Nrf2 exacerbates cardiac hypertrophy, inflammation, fibrosis and oxidative stress in cultured cardiomyocytes and Nrf2-deficient mice. 23,25 Therefore, Nrf2 is considered to be a promising drug target for preventing heart damage caused by Ang II.…”

“…[23][24][25] The overexpression of Nrf2 inhibits cardiomyopathy and ROS produced by Ang II administration, whereas the absence of Nrf2 exacerbates cardiac hypertrophy, inflammation, fibrosis and oxidative stress in cultured cardiomyocytes and Nrf2-deficient mice. 23,25 Therefore, Nrf2 is considered to be a promising drug target for preventing heart damage caused by Ang II. Sulforaphane (SFN) is a naturally occurring isothiocyanate compound extracted from broccoli sprouts.…”

The protective effects of the miR-129-5p/keap-1/Nrf2 axis on Ang II-induced cardiomyocyte hypertrophy

“…Nuclear factor erythroid2-related factor 2 (Nrf2) is an important transcription factor that regulates antioxidant stress and plays a cardiac protection role (14). Chen et al found that Nrf2 deficiency aggravated Ang II-induced cardiac injury by increasing hypertrophy and enhancing inflammation (15). The Kelch-like ECH-associated protein 1 (Keap1), an intracellular sensor for oxidative stress, is a specific receptor for Nrf2 that mediates the degradation of Nrf2 through ubiquitination (16).…”

Increased ketohexokinase-A governs fructose-induced podocyte hypertrophy by IL-6/STAT3 signaling activation

“…Addition of exogenous recombinant IL-6 is reported to activate signal transducer and activator of transcription 3 (STAT3) in primary cultured podocytes (Henique et al, 2017). Activation of IL-6/STAT3 signaling is detected in angiotensin II-induced hypertrophic cardiomyopathy mice with cardiac inflammation and hypertrophy (Chen et al, 2019). These observations indicate that IL-6/STAT3 activation may promote podocyte hypertrophy.…”