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.

Základní údaje

Originální název

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

Autoři

MANOUSEK, Jan (203 Česká republika), Petr KALA (203 Česká republika, domácí), Petr LOKAJ (203 Česká republika, domácí), Tomáš ONDRÚŠ (703 Slovensko, domácí), Kateřina HELÁNOVÁ (203 Česká republika, domácí), Marie MIKLÍKOVÁ (203 Česká republika), Vojtěch BRÁZDIL (203 Česká republika, domácí), Marie TOMANDLOVÁ (203 Česká republika, domácí), Jiří PAŘENICA (203 Česká republika, domácí), Monika PÁVKOVÁ GOLDBERGOVÁ (203 Česká republika, domácí) a Jiří HLÁSENSKÝ (203 Česká republika, garant, domácí)

Vydání

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

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30201 Cardiac and Cardiovascular systems

Stát vydavatele

Švýcarsko

Utajení

není předmětem státního či obchodního tajemství

Odkazy

Impakt faktor

Impact factor: 5.846

Kód RIV

RIV/00216224:14110/21:00123225

Organizační jednotka

Lékařská fakulta

UT WoS

000715825000001

Klíčová slova anglicky

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

Příznaky

Mezinárodní význam, Recenzováno
Změněno: 28. 8. 2024 10:36, Mgr. Michal Petr

Anotace

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.