Inhibition of Autophagy by Chloroquine Stimulates Nitric Oxide Production and Protects Endothelial Function during Serum Deprivation | Zendy

Cezar Rangel Pestana | Zendy; Jorge Oishi | Zendy; Heloísa Sobreiro Salistre-Araújo | Zendy; Gerson Jhonatan Rodrigues | Zendy

Open Access

Inhibition of Autophagy by Chloroquine Stimulates Nitric Oxide Production and Protects Endothelial Function during Serum Deprivation

Author(s) -

Cezar Rangel Pestana,

Jorge Oishi,

Heloísa Sobreiro Salistre-Araújo,

Gerson Jhonatan Rodrigues

Publication year - 2015

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000430240

Subject(s) - autophagy , autophagosome , microbiology and biotechnology , nitric oxide , sequestosome 1 , endothelium , chemistry , endothelial stem cell , lysosome , chloroquine , pharmacology , biology , apoptosis , biochemistry , endocrinology , immunology , in vitro , enzyme , malaria

Autophagy plays a fundamental role in cell survival under stress conditions such as nutrient deprivation. Decreased nitric oxide (NO) production, which may contribute to vascular dysfunction, is one of the consequences of autophagy in endothelial cells. The antimalarial drug chloroquine (CLQ) inhibits autophagy by blocking autophagosome formation and has been proposed as adjuvant chemotherapy in other diseases.

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