Dear Editor,

Atrial natriuretic peptide (ANP), a hormone mainly produced by cardiomyocytes and interacting with specific receptors located within the plasma membrane of target cells, plays an important role in several renal and cardiovascular mechanisms.1 Two major subtypes of ANP receptors have been characterized: NPR-A receptors, which activate guanylate cyclase (GC), giving rise to cyclic GMP after binding ANP at pharmacological concentrations (10−6–10−8 M), and NPR-C receptors, which modulate intracellular cAMP or membrane lipid turnover through the activation of specific phospholipases1, 2 after binding the hormone at physiological concentrations (10−9–10−11 M). The presence of ANP receptors in different organs and tissues, including lung and liver,1 has been related to the ANP ability to negatively regulate cell growth by different pathways.3 Among others also the membrane-bound NADPH oxidase plays an important role in cell growth regulation through the production of reactive oxygen species (ROS). The enzyme activation proceeds at the plasma membrane level through a multistep assembly of several cytosolic factors and small GTP-binding proteins, such as Rap1A and Rac.4 In particular, in HepG2 cells, NADPH oxidase Rac1 subunit is involved in the generation of ROS, which, when in excess, can switch apoptosis to necrosis by the inhibition of caspase-3.5 To identify a possible link between ANP, ROS production and cell growth, we analyzed in more detail the role of ANP in cell death mechanisms and the possible relationship between the physiological concentration (10–10 M) of ANP and ROS production in HepG2 cells.

Log in or create a free account to read this content

Gain free access to this article, as well as selected content from this journal and more on nature.com

Access through your institution

or

Sign in or create an account
Continue with Google
Continue with ORCiD