Oxidative stress and cardiomyocyte necrosis with elevated serum troponins

Pathophysiologic mechanisms

Antwon D. Robinson, K Ramanathan, Jesse E. McGee, Kevin P. Newman, Karl Weber

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

The progressive nature of heart failure is linked to multiple factors, including an ongoing loss of cardiomyocytes and necrosis. Necrotic cardiomyocytes leave behind several footprints: the spillage of their contents leading to elevations in serum troponins; and morphologic evidence of tissue repair with scarring. The pathophysiologic origins of cardiomyocyte necrosis relates to neurohormonal activation, including the adrenergic nervous system. Catecholamine-initiated excessive intracellular Ca2+ accumulation and mitochondria Ca2+ overloading in particular initiate a mitochondriocentric signal-transducer-effector pathway to necrosis and which includes the induction of oxidative stress and opening of their inner membrane permeability transition pore. Hypokalemia, ionized hypocalcemia and hypomagnesemia, where consequent elevations in parathyroid hormone further account for excessive intracellular Ca accumulation, hypozincemia and hyposelenemia each compromise metalloenzyme-based antioxidant defenses. The necrotic loss of cardiomyocytes and adverse structural remodeling of myocardium is related to the central role played by a mitochondriocentric pathway initiated by neurohormonal activation.

Original languageEnglish (US)
Pages (from-to)129-134
Number of pages6
JournalAmerican Journal of the Medical Sciences
Volume342
Issue number2
DOIs
StatePublished - Jan 1 2011

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Troponin
Cardiac Myocytes
Oxidative Stress
Necrosis
Serum
Hypokalemia
Hypocalcemia
Transducers
Parathyroid Hormone
Adrenergic Agents
Nervous System
Catecholamines
Cicatrix
Permeability
Myocardium
Mitochondria
Heart Failure
Antioxidants
Membranes

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Oxidative stress and cardiomyocyte necrosis with elevated serum troponins : Pathophysiologic mechanisms. / Robinson, Antwon D.; Ramanathan, K; McGee, Jesse E.; Newman, Kevin P.; Weber, Karl.

In: American Journal of the Medical Sciences, Vol. 342, No. 2, 01.01.2011, p. 129-134.

Research output: Contribution to journalArticle

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