SK channel enhancers attenuate Ca 2+ -dependent arrhythmia in hypertrophic hearts by regulating mito-ROS-dependent oxidation and activity of RyR

ConclusionThese data suggest that enhancement of mSK channels in hypertrophic rat hearts protects from Ca2+-dependent arrhythmia and suggest that the protection is mediated via decreased mitochondrial ROS and subsequent decreased oxidation of reactive cysteines in RyR, which ultimately leads to stabilization of RyR-mediated Ca2+ release.
Source: Cardiovascular Research - Category: Cardiology Source Type: research

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We report a case of migration of arterial stent, placed in the right iliac vein into the right pulmonary artery which was diagnosed there and subsequently not removed for at least 3 years. Despite reports in the literature for the removal of migrated stents by mini-invasive interventional methods, in our case, this was not possible, because of the long period for which the foreign body was in the right pulmonary artery and the proximal partial occlusion of organized mural thrombus.
Source: The Annals of Thoracic Surgery - Category: Cardiovascular & Thoracic Surgery Source Type: research
We report a patient carrying a novel pathogenic variant p.(Tyr101Cys) in ISCA1 leading to MMDS type 5. He initially presented a psychomotor regression with loss of gait and language skills and a tetrapyramidal spastic syndrome. Biochemical analysis of patient fibroblasts revealed impaired lipoic acid synthesis and decreased activities of complex I and II of respiratory chain. While ISCA1 is involved in mitochondrial machinery of iron-sulfur cluster biogenesis, these dysfunctions are secondary to impaired maturation of mitochondrial proteins containing the [4Fe-4S] clusters. Expression and purification of the human ISCA1 sh...
Source: Mitochondrion - Category: Biochemistry Source Type: research
Publication date: March 2020Source: European Journal of Surgical Oncology, Volume 46, Issue 3Author(s): Sara Hägg, Juulia JylhäväAbstractColorectal cancer (CRC) is a chronic disease of the old population with slow development progressing into clinical signs and symptoms. Biological aging is characterized by e.g. mitochondrial dysfunction and epigenetic alterations (e.g. methylation) - mechanisms that are also important in cancer development. For CRC, specific types of tumors are distinguishable by their methylation patterns and several detection methods using different epigenetic marks have been developed as...
Source: European Journal of Surgical Oncology (EJSO) - Category: Surgery Source Type: research
ConclusionsFindings might have implications for targeting both psychological control and emotion regulation difficulties in personalized anxiety interventions during this high-risk developmental period.
Source: Journal of Behavior Therapy and Experimental Psychiatry - Category: Psychiatry Source Type: research
Publication date: Available online 21 February 2020Source: Clinica Chimica ActaAuthor(s): Anbo Gao, Jinyong Jiang, Feng Xie, Linxi ChenAbstractThe present review is a summary of the recent literature concerning Bnip3 expression, function, and regulation, along with its implications in mitochondrial dysfunction, disorders of mitophagy homeostasis, and development of diseases of secondary mitochondrial dysfunction. As a member of the Bcl-2 family of cell death-regulating factors, Bnip3 mediates mPTP opening, mitochondrial potential, oxidative stress, calcium overload, mitochondrial respiratory collapse, and ATP shortage of m...
Source: Clinica Chimica Acta - Category: Laboratory Medicine Source Type: research
Conclusions: We demonstrated for the first time the feasibility of noninvasive, in vivo, quantitative assessment of cardiac T in humans. Quantitative values of T are in good agreement with bench top measurements in isolated mitochondria, cells and Langendorff perfused rat hearts (see Alpert et al, 2018). Currently, there are no methods for direct in vivo assessment of mitochondrial function. In vivo quantification of the mitochondrial function could provide new diagnostic and prognostic information for several cardiac diseases as well as allowing therapy monitoring. Further investigations are required to assess these poten...
Source: Journal of Nuclear Medicine - Category: Nuclear Medicine Authors: Tags: Cardiovascular YIA Symposium Source Type: research
In conclusion, we here demonstrate how a complex pattern of many modest changes at gene level may explain major functional differences of the action potential related to ageing and mitochondrial dysfunction. PMID: 30914453 [PubMed - as supplied by publisher]
Source: Bioscience Reports - Category: Biomedical Science Authors: Tags: Biosci Rep Source Type: research
ConclusionThese results suggest a novel pharmacological pathway of n-3 PUFAs and suggest that their well-known cardioprotective effects are mediated by their oxygenated metabolites such as NeuroPs.
Source: Archives of Cardiovascular Diseases Supplements - Category: Cardiology Source Type: research
Conclusions Here we suggest that the FK506-induced calcium overload promotes mitochondrial calcium accumulation and leads to mPTP opening. We propose that mPTP opening should be considered as an arrhythmogenic substrate. The author hereby declares no conflict of interest
Source: Archives of Cardiovascular Diseases Supplements - Category: Cardiology Source Type: research
Publication date: May 2015 Source:Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Volume 1852, Issue 5 Author(s): J. Roussel , J. Thireau , C. Brenner , N. Saint , V. Scheuermann , A. Lacampagne , J.-Y. Le Guennec , J. Fauconnier Long chain fatty acids bind to carnitine and form long chain acyl carnitine (LCAC), to enter into the mitochondria. They are oxidized in the mitochondrial matrix. LCAC accumulates rapidly under metabolic disorders, such as acute cardiac ischemia, chronic heart failure or diabetic cardiomyopathy. LCAC accumulation is associated with severe cardiac arrhythmia including ventricula...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - Category: Molecular Biology Source Type: research
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