J 2021

Oxidative Stress in Takotsubo Syndrome-Is It Essential for an Acute Attack? Indirect Evidences Support Multisite Impact Including the Calcium Overload-Energy Failure Hypothesis

MANOUSEK, Jan, Petr KALA, Petr LOKAJ, Tomáš ONDRÚŠ, Kateřina HELÁNOVÁ et. al.

Basic information

Original name

Oxidative Stress in Takotsubo Syndrome-Is It Essential for an Acute Attack? Indirect Evidences Support Multisite Impact Including the Calcium Overload-Energy Failure Hypothesis

Authors

MANOUSEK, Jan (203 Czech Republic), Petr KALA (203 Czech Republic, belonging to the institution), Petr LOKAJ (203 Czech Republic, belonging to the institution), Tomáš ONDRÚŠ (703 Slovakia, belonging to the institution), Kateřina HELÁNOVÁ (203 Czech Republic, belonging to the institution), Marie MIKLÍKOVÁ (203 Czech Republic), Vojtěch BRÁZDIL (203 Czech Republic, belonging to the institution), Marie TOMANDLOVÁ (203 Czech Republic, belonging to the institution), Jiří PAŘENICA (203 Czech Republic, belonging to the institution), Monika PÁVKOVÁ GOLDBERGOVÁ (203 Czech Republic, belonging to the institution) and Jiří HLÁSENSKÝ (203 Czech Republic, guarantor, belonging to the institution)

Edition

FRONTIERS IN CARDIOVASCULAR MEDICINE, LAUSANNE, FRONTIERS MEDIA SA, 2021, 2297-055X

Other information

Language

English

Type of outcome

Článek v odborném periodiku

Field of Study

30201 Cardiac and Cardiovascular systems

Country of publisher

Switzerland

Confidentiality degree

není předmětem státního či obchodního tajemství

References:

Impact factor

Impact factor: 5.846

RIV identification code

RIV/00216224:14110/21:00123225

Organization unit

Faculty of Medicine

UT WoS

000715825000001

Keywords in English

Takotsubo syndrome; oxidative stress; catecholamines; cytochrome P450; sarco(endo)plasmic reticulum; mitochondria complex; calcium overload; energy failure; antioxidants

Tags

International impact, Reviewed
Změněno: 28/8/2024 10:36, Mgr. Michal Petr

Abstract

V originále

Indirect evidences in reviews and case reports on Takotsubo syndrome (TTS) support the fact that the existence of oxidative stress (OS) might be its common feature in the pre-acute stage. The sources of OS are exogenous (environmental factors including pharmacological and toxic influences) and endogenous, the combination of both may be present, and they are being discussed in detail. OS is associated with several pathological conditions representing TTS comorbidities and triggers. The dominant source of OS electrones are mitochondria. Our analysis of drug therapy related to acute TTS shows many interactions, e.g., cytostatics and glucocorticoids with mitochondrial cytochrome P450 and other enzymes important for OS. One of the most frequently discussed mechanisms in TTS is the effect of catecholamines on myocardium. Yet, their metabolic influence is neglected. OS is associated with the oxidation of catecholamines leading to the synthesis of their oxidized forms - aminochromes. Under pathological conditions, this pathway may dominate. There are evidences of interference between OS, catecholamine/aminochrome effects, their metabolism and antioxidant protection. The OS offensive may cause fast depletion of antioxidant protection including the homocystein-methionine system, whose activity decreases with age. The alteration of effector subcellular structures (mitochondria, sarco/endoplasmic reticulum) and subsequent changes in cellular energetics and calcium turnover may also occur and lead to the disruption of cellular function, including neurons and cardiomyocytes. On the organ level (nervous system and heart), neurocardiogenic stunning may occur. The effects of OS correspond to the effect of high doses of catecholamines in the experiment. Intensive OS might represent "conditio sine qua non" for this acute clinical condition. TTS might be significantly more complex pathology than currently perceived so far.