Detail
Article
Online article
FT
Medvik - BMC
  • Something wrong with this record ?

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

J. Manousek, P. Kala, P. Lokaj, T. Ondrus, K. Helanova, M. Miklikova, V. Brazdil, M. Tomandlova, J. Parenica, M. Pavkova Goldbergova, J. Hlasensky

. 2021 ; 8 (-) : 732708. [pub] 20211019

Language English Country Switzerland

Document type Journal Article

Persistent link   https://www.medvik.cz/link/bmc22001511

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.

References provided by Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc22001511
003      
CZ-PrNML
005      
20220112153627.0
007      
ta
008      
220107s2021 sz f 000 0|eng||
009      
AR
024    7_
$a 10.3389/fcvm.2021.732708 $2 doi
035    __
$a (PubMed)34738019
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a sz
100    1_
$a Manousek, Jan $u Department of Internal Medicine and Cardiology, University Hospital Brno, Brno, Czechia
245    10
$a Oxidative Stress in Takotsubo Syndrome-Is It Essential for an Acute Attack? Indirect Evidences Support Multisite Impact Including the Calcium Overload-Energy Failure Hypothesis / $c J. Manousek, P. Kala, P. Lokaj, T. Ondrus, K. Helanova, M. Miklikova, V. Brazdil, M. Tomandlova, J. Parenica, M. Pavkova Goldbergova, J. Hlasensky
520    9_
$a 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.
655    _2
$a časopisecké články $7 D016428
700    1_
$a Kala, Petr $u Department of Internal Medicine and Cardiology, University Hospital Brno, Brno, Czechia $u Department of Internal Medicine and Cardiology, Faculty of Medicine, Masaryk University, Brno, Czechia
700    1_
$a Lokaj, Petr $u Department of Internal Medicine and Cardiology, University Hospital Brno, Brno, Czechia $u Department of Internal Medicine and Cardiology, Faculty of Medicine, Masaryk University, Brno, Czechia
700    1_
$a Ondrus, Tomas $u Department of Internal Medicine and Cardiology, University Hospital Brno, Brno, Czechia $u Department of Internal Medicine and Cardiology, Faculty of Medicine, Masaryk University, Brno, Czechia
700    1_
$a Helanova, Katerina $u Department of Internal Medicine and Cardiology, University Hospital Brno, Brno, Czechia $u Department of Internal Medicine and Cardiology, Faculty of Medicine, Masaryk University, Brno, Czechia
700    1_
$a Miklikova, Marie $u Department of Internal Medicine and Cardiology, University Hospital Brno, Brno, Czechia
700    1_
$a Brazdil, Vojtech $u Department of Internal Medicine and Cardiology, University Hospital Brno, Brno, Czechia $u Department of Internal Medicine and Cardiology, Faculty of Medicine, Masaryk University, Brno, Czechia
700    1_
$a Tomandlova, Marie $u Department of Biochemistry, Faculty of Medicine, Masaryk University, Brno, Czechia
700    1_
$a Parenica, Jiri $u Department of Internal Medicine and Cardiology, University Hospital Brno, Brno, Czechia $u Department of Internal Medicine and Cardiology, Faculty of Medicine, Masaryk University, Brno, Czechia
700    1_
$a Pavkova Goldbergova, Monika $u Department of Pathophysiology, Faculty of Medicine, Masaryk University, Brno, Czechia
700    1_
$a Hlasensky, Jiri $u Department of Internal Medicine and Cardiology, University Hospital Brno, Brno, Czechia $u Department of Internal Medicine and Cardiology, Faculty of Medicine, Masaryk University, Brno, Czechia
773    0_
$w MED00198704 $t Frontiers in cardiovascular medicine $x 2297-055X $g Roč. 8, č. - (2021), s. 732708
856    41
$u https://pubmed.ncbi.nlm.nih.gov/34738019 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y - $z 0
990    __
$a 20220107 $b ABA008
991    __
$a 20220112153623 $b ABA008
999    __
$a ind $b bmc $g 1745508 $s 1152658
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2021 $b 8 $c - $d 732708 $e 20211019 $i 2297-055X $m Frontiers in cardiovascular medicine $n Front Cardiovasc Med $x MED00198704
LZP    __
$a Pubmed-20220107

Find record

Citation metrics

Archiving options