ArticleJournal of cardiovascular pharmacology2010
Uncoupling the coupled calcium and zinc dyshomeostasis in cardiac myocytes and mitochondria seen in aldosteronism.
Article in Journal of cardiovascular pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Heart Failure and Osteoporosis: Shared Challenges in the Aging Population.Journal of cardiovascular development and disease · 2025Review
- Cardiovascular Disease in Obstructive Sleep Apnea: Putative Contributions of Mineralocorticoid Receptors.International journal of molecular sciences · 2023Review
- Micronutrient deficiencies in heart failure: Mitochondrial dysfunction as a common pathophysiological mechanism?Journal of internal medicine · 2022Review
- Bone in heart failure.Journal of cachexia, sarcopenia and muscle · 2020Review
- Impact of Labile Zinc on Heart Function: From Physiology to Pathophysiology.International journal of molecular sciences · 2017Review
- Influence of renal impairment on aldosterone status, calcium metabolism, and vasopressin activity in outpatients with systolic heart failure.ESC heart failure · 2017Article
- Atrophied cardiomyocytes and their potential for rescue and recovery of ventricular function.Heart failure reviews · 2016Review
- Zinc and the prooxidant heart failure phenotype.Journal of cardiovascular pharmacology · 2014Review
- Small dedifferentiated cardiomyocytes bordering on microdomains of fibrosis: evidence for reverse remodeling with assisted recovery.Journal of cardiovascular pharmacology · 2014Article
- Enhancement of cellular antioxidant-defence preserves diastolic dysfunction via regulation of both diastolic Zn2+ and Ca2+ and prevention of RyR2-leak in hyperglycemic cardiomyocytes.Oxidative medicine and cellular longevity · 2014Article
- Gene Expression Profiles of Peripheral Blood Mononuclear Cells Reveal Transcriptional Signatures as Novel Biomarkers for Cardiac Remodeling in Rats with Aldosteronism and Hypertensive Heart Disease.JACC. Heart failure · 2013Article
- Atrophic cardiomyocyte signaling in hypertensive heart disease.Journal of cardiovascular pharmacology · 2013Article
- Mineralocorticoid receptor antagonism confers cardioprotection in heart failure.Current heart failure reports · 2013Review
- Heart failure as a risk factor for osteoporosis and fractures.Current osteoporosis reports · 2012Review
- Mitochondria play a central role in nonischemic cardiomyocyte necrosis: common to acute and chronic stressor states.Pflugers Archiv : European journal of physiology · 2012Review
- Cation dyshomeostasis and cardiomyocyte necrosis: the Fleckenstein hypothesis revisited.European heart journal · 2011Article
- Mitochondriocentric pathway to cardiomyocyte necrosis in aldosteronism: cardioprotective responses to carvedilol and nebivolol.Journal of cardiovascular pharmacology · 2011Article
- Calcium and zinc dyshomeostasis during isoproterenol-induced acute stressor state.American journal of physiology. Heart and circulatory physiology · 2011Article
- Cellular and molecular pathways to myocardial necrosis and replacement fibrosis.Heart failure reviews · 2011Review
- Intracellular calcium overloading and oxidative stress in cardiomyocyte necrosis via a mitochondriocentric signal-transducer-effector pathway.Experimental and clinical cardiology · 2011Article
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
Intracellular [Ca2+]i overloading in cardiomyocytes is a fundamental pathogenic event associated with chronic aldosterone/salt treatment (ALDOST) and accounts for an induction of oxidative stress that leads to necrotic cell death and consequent myocardial scarring. This prooxidant response to Ca2+ overloading in cardiac myocytes and mitochondria is intrinsically coupled to simultaneous increased Zn2+ entry serving as an antioxidant. Herein, we investigated whether Ca2+ and Zn2+ dyshomeostasis and prooxidant to antioxidant dysequilibrium seen at 4 weeks, the pathologic stage of ALDOST, could be uncoupled in favor of antioxidants, using cotreatment with a ZnSO4 supplement; pyrrolidine dithiocarbamate (PDTC), a Zn2+ ionophore; or ZnSO4 in combination with amlodipine (Amlod), a Ca2+ channel blocker. We monitored and compared responses in cardiomyocyte free [Ca2+]i and [Zn2+]i together with biomarkers of oxidative stress in cardiac myocytes and mitochondria. At week 4 of ALDOST and compared with controls, we found (1) an elevation in [Ca2+]i coupled with [Zn2+]i and (2) increased mitochondrial H2O2 production and increased mitochondrial and cardiac 8-isoprostane levels. Cotreatment with the ZnSO4 supplement alone, PDTC, or ZnSO4+Amlod augmented the rise in cardiomyocyte [Zn2+]i beyond that seen with ALDOST alone, whereas attenuating the rise in [Ca2+]i, which together served to reduce oxidative stress. Thus, a coupled dyshomeostasis of intracellular Ca2+ and Zn2+ was demonstrated in cardiac myocytes and mitochondria during 4-week ALDOST, where prooxidants overwhelm antioxidant defenses. This intrinsically coupled Ca2+ and Zn2+ dyshomeostasis could be uncoupled in favor of antioxidant defenses by selectively increasing free [Zn2+]i and/or reducing [Ca2+]i using cotreatment with ZnSO4 or PDTC alone or ZnSO4+Amlod in combination.
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