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Nrf2 deficiency aggravates PM_2.5-induced cardiomyopathy by enhancing oxidative stress, fibrosis and inflammation via RIPK3-regulated mitochondrial disorder.

ABSTRACT: PM_2.5 is a well-known air pollutant threatening public health, and long-term exposure to PM_2.5 increases the risk of cardiovascular diseases. Nrf2 plays a pivotal role in the amelioration of PM_2.5-induced lung injury. However, if Nrf2 is involved in PM_2.5-induced heart injury, and the underlying molecular mechanisms have not been explored. In this study, wild type (Nrf2^+/+) and Nrf2 knockout (Nrf2^-/-) mice were exposed to PM_2.5 for 6 months. After PM_2.5 exposure, Nrf2^-/- mice developed severe physiological changes, lung injury and cardiac dysfunction. In the PM_2.5-exposed hearts, Nrf2 deficiency caused significant collagen accumulation through promoting the expression of fibrosis-a

SUBMITTER: Ge C

PROVIDER: S-EPMC7138545 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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Nrf2 deficiency aggravates PM_2.5-induced cardiomyopathy by enhancing oxidative stress, fibrosis and inflammation via RIPK3-regulated mitochondrial disorder.

OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

Nrf2 deficiency aggravates PM2.5-induced cardiomyopathy by enhancing oxidative stress, fibrosis and inflammation via RIPK3-regulated mitochondrial disorder.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Nrf2 deficiency aggravates PM_2.5-induced cardiomyopathy by enhancing oxidative stress, fibrosis and inflammation via RIPK3-regulated mitochondrial disorder.