Track topics on Twitter Track topics that are important to you
A growing body of data provides strong evidence that intracellular angiotensin II (Ang II) plays an important role in mammalian cell function and is involved in the pathogenesis of human diseases such hypertension, diabetes, inflammation, fibrosis, arrhythmias, and kidney disease, among others. Recent studies also suggest that intracellular Ang II exert protective effects in cells during high extracellular levels of the hormone or during chronic stimulation of local tissue renin-angiotensin system (RAS). Notably, the intracellular RAS (iRAS) described in neurons, fibroblasts, renal cells, and cardiomyocytes, have provided new insights into regulatory mechanisms mediated by intracellular Ang II type 1 (AT1-Rs) and 2 receptors (AT2-Rs), particularly, in mitochondria and nucleus. Ang II through nuclear AT1-Rs promotes protective mechanisms by stimulating the AT2-R signaling cascade which involves mitochondrial AT2-Rs and Mas receptors. The stimulation of nuclear Ang II receptors enhances mitochondrial biogenesis, thus protecting the cell against oxidative stress. Recent studies in Ang II-induced preconditioning suggest that plasma membrane AT2-R stimulation exerts protective effects against cardiac ischemia-reperfusion by modulating mitochondrial AT1-R and AT-2R signaling. These studies suggest that iRAS promotes the protection of cells through nuclear AT1-R signaling, which, in turn, promotes AT2-R-dependent processes in mitochondria. Thus, despite abundant data on the deleterious effects of intracellular Ang II, a growing body of studies also support a protective role for iRAS. This review summarizes and discusses previous studies on the role of iRAS, particularly, emphasizing the protective and counterbalancing actions of iRAS, mitochondrial Ang II receptors, and their implications for organ protection.
This article was published in the following journal.
Name: American journal of physiology. Heart and circulatory physiology
The renin-angiotensin system promotes oxidative stress, apoptosis, necrosis, fibrosis, and thus heart failure. Secretory renin plays a central role in these processes, initiating the generation of ang...
Impaired mitochondrial function and activation of NLRP3 inflammasomes cascade has a significant role in the pathogenesis of myocardial ischemia-reperfusion (IR) injury. The current study investigated ...
Renin angiotensin system (RAS) blockers are in clinical use to treat high blood pressure and proteinuric chronic kidney disease. However, RAS blockade is limited by the risk of hyperkalemia, angiotens...
The mitochondrial permeability transition pore opening plays a critical role in the pathogenesis of myocardial infarction. Inhibition of cyclophilin-D (CyP-D), a key regulator of the mitochondrial per...
Mitochondria possess elaborate machineries for the import of proteins from the cytosol. Cytosolic factors like Hsp70 chaperones and their co-chaperones, the J-proteins, guide proteins to the mitochond...
This study is designed to evaluate specific factors in mitochondria that may precipitate premature aging and physical weakness in HIV patients. Angiotensin receptors 1 and 2 (AT1R and AT2R...
The renin angiotensin system is a complex process involving hormones and enzymes that regulate blood volume and blood pressure. The hormone angiotensin II is responsible for making blood ...
The overall aim of this study is to examine the role of mitochondrial respiration in human diabetic tissue before and after ischemia. Furthermore we will examine the ability of ischemic pr...
An angiotensin II type 2 receptor (AT2R) antagonist has been assessed for its efficacy in neuropathic pain with promising results. A considerable number of patients undergoing surgery unde...
It is well known that atrial fibrillation (AF) and atrial flutter (Aflut) occur frequently after most types of cardiac surgeries.(1-4) Postoperative AF is associated with significant morbi...
Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.
A decapeptide that is cleaved from precursor angiotensinogen by RENIN. Angiotensin I has limited biological activity. It is converted to angiotensin II, a potent vasoconstrictor, after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME.
An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.
A heptapeptide formed from ANGIOTENSIN II after the removal of an amino acid at the N-terminal by AMINOPEPTIDASE A. Angiotensin III has the same efficacy as ANGIOTENSIN II in promoting ALDOSTERONE secretion and modifying renal blood flow, but less vasopressor activity (about 40%).
An ANGIOTENSIN II analog which acts as a highly specific inhibitor of ANGIOTENSIN TYPE 1 RECEPTOR.
Pulmonary arterial hypertension (PAH) is a chronic, life-threatening disorder characterized by abnormally high blood pressure in the arteries between the heart and lungs of affected individuals. Symptoms can range from mild breathles...