Fig. 7: ALDH2 protects angiotensin II-induced hypertrophic response via Nrf1-FUNDC1-dependent pathway. | Cell Death & Disease

Fig. 7: ALDH2 protects angiotensin II-induced hypertrophic response via Nrf1-FUNDC1-dependent pathway.

From: Alpha-lipoic acid protects against pressure overload-induced heart failure via ALDH2-dependent Nrf1-FUNDC1 signaling

Fig. 7

a, b Correlation between ALDH2 and Nrf1 expression as well as FUNDC1 and Nrf1 in GTEx database; c Western blots of Nrf1, Nrf2, PFKP, LDHA, and β-actin in tissue (loading control) (n = 6 samples per group); d Western blots of ALDH2, FUNDC1, Nrf1, and β-actin (loading control) in NRCMs after transfection (n = 6 samples per group); e depiction of the putative Nrf1-binding site located at FUNDC1 promoter; f predicted potential Nrf1REs; g chromatin immunoprecipitation (ChIP) assay in NRCMs; h construction pGL3 luciferase reporter vector with FUNDC1 promoter; i luciferase assay in NRCMs (n = 6 samples per group); j schematic diagram depicting the role of α-LA in pressure overload-induced changes in ALDH2 and mitophagy. Pressure overload suppresses expression and activity of myocardium ALDH2, which participates in pressure overload-induced inhibition of mitophagy receptor FUNDC1 and LC3II. Besides, the beneficial effects of α-LA in pressure overload heart failure was mediated by a novel ALDH2–Nrf1–FUNDC1 signaling pathway in which procedure Nrf1 modulates the FUNDC1 expression via directly binding to the 5′ promoter of FUNDC1. Mean ± SEM, ***P < 0.001. Statistical analysis was carried out by a two-tailed Student’s t test analysis.

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