Candesartan cilexetil protects from cardiac myosin induced cardiotoxicity via reduction of endoplasmic reticulum stress and apoptosis in rats: Involvement of ACE2-Ang (1–7)- mas axis

• Published in: Toxicology (Amsterdam) Vol. 291; no. 1-3; pp. 139 - 145
• Main Authors: Arumugam, Somasundaram, Thandavarayan, Rajarajan A, Palaniyandi, Suresh S, Giridharan, Vijayasree V, Arozal, Wawaimuli, Sari, Flori R, Soetikno, Vivian, Harima, Meilei, Suzuki, Kenji, Kodama, Makoto, Watanabe, Kenichi
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier Ireland Ltd 27.01.2012; Elsevier
• Subjects: Ang (1–7); Angiotensin I - pharmacology; Angiotensin II - biosynthesis; Angiotensin II Type 1 Receptor Blockers - pharmacology; animal models; Animals; apoptosis; Apoptosis - drug effects; Apoptosis Regulatory Proteins - biosynthesis; Autoimmune Diseases - chemically induced; Autoimmune Diseases - prevention & control; Benzimidazoles - pharmacology; Biological and medical sciences; Biphenyl Compounds - pharmacology; Blotting, Western; calcium; Candesartan cilexetil; Cardiology. Vascular system; cardiomyopathy; Cardioprotection; Cell Survival - drug effects; Emergency; endoplasmic reticulum; Endoplasmic Reticulum Stress - drug effects; Heart; Heart Diseases - chemically induced; Heart Diseases - prevention & control; Heart failure; Heart failure, cardiogenic pulmonary edema, cardiac enlargement; histopathology; homeostasis; immunization; Immunohistochemistry; In Situ Nick-End Labeling; Male; mas; Medical sciences; Myocarditis - chemically induced; Myocarditis - prevention & control; myocardium; myosin; Myosins - antagonists & inhibitors; Myosins - toxicity; Peptide Fragments - pharmacology; Peptidyl-Dipeptidase A - metabolism; Proto-Oncogene Proteins - physiology; Rats; Rats, Inbred Lew; receptors; Receptors, G-Protein-Coupled - physiology; Sarcoplasmic Reticulum Calcium-Transporting ATPases - biosynthesis; Signal Transduction - physiology; swine; Tetrazoles - pharmacology; Toxicology; Western blotting; Heart failure; Candesartan cilexetil; Cardioprotection; Ang (1–7); mas; Heart; Imidazole derivatives; Tetrazole derivatives; Rat; Candesartan; Toxicity; Peptide hormone; Contractile protein; Cardiovascular disease; Prevention; Octapeptide; Reduction; Ang (1-7) mas; Heart disease; Myosin; Angiotensin II; Mechanism of action; Cilexetil; Rodentia; Cardioprotective agent; Stress; Mass; Renin angiotensin system; Vertebrata; Mammalia; Biphenyl derivatives; Cell death; Animal; Antihypertensive agent; Sartan derivatives; Angiotensin antagonist; Circulatory system; Endoplasmic reticulum; Apoptosis
• ISSN: 0300-483X; 1879-3185
• DOI: 10.1016/j.tox.2011.11.008

Highlights ► EAM progression involves endoplasmic reticulum stress and cardiomyocyte apoptosis. ► ACE2-Ang (1–7)- mas axis is modulated during this condition. ► Candesartan cilexetil prevented the progression of EAM to dilated cardiomyopathy. ► Candesartan cilexetil reversed the change in SERCA2 expression in DCM.