Mitochondrial Pathophysiology

Ischemia-reperfusion (IR) injury occurs when the blood supply to an organ is interrupted and then restored. IR injury is mainly caused by calcium overload, oxidative stress and mitochondrial dysfuntion. We are studying the molecular and cellular mechanisms that confer ischemia tolerance and protect against IR injury. Currently, we focus on the antioxidant transcription factor Nrf2 (NF-E2-related factor 2), a master regulator of the cellular redox homeostasis, as well as in the PI3K/Akt and ERK1/2 signalling pathways. In this project, we will study the contribution of these pathways to cardioprotection in cultured cardiomyocytes using a combination of biochemistry, molecular biology and cell biology techniques.

Recent publications

- Cadenas S (2018) Mitochondrial uncoupling, ROS generation and cardioprotection. Biochim. Biophys. Acta 1859, 940-950.

-  Cadenas S (2018) ROS and redox signaling in myocardial ischemia-reperfusion injury and cardioprotection. Free Radic. Biol. Med. 117, 76-89.

- López-Bernardo E, Anedda A, Sánchez-Pérez P, Acosta-Iborra B, Cadenas S (2015) 4-Hydroxynonenal induces Nrf2-mediated UCP3 upregulation in mouse cardiomyocytes. Free Radic. Biol. Med. 88, 427-438.

- Espinosa-Diez C, Miguel V, Mennerich D, Kietzmann T, Sánchez-Pérez P, Cadenas S, Lamas S (2015) Antioxidant responses and cellular adjustments to oxidative stress. Redox Biol. 6, 183-197.

- Anedda A, López-Bernardo E, Acosta-Iborra B, Suleiman MS, Landázuri MO, Cadenas S (2013) The transcription factor Nrf2 promotes survival by enhancing the expression of uncoupling protein 3 under conditions of oxidative stress. Free Radic. Biol. Med. 61, 395-407.