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A Genetic Variant of miR-34a Contributes to Susceptibility of Ischemic Stroke Among Chinese Population
This study was supported by National Natural Science Foundation of China (Nos. 81560552, 81260234), Natural Science Foundation of Guangxi Zhuang Autonomous Region (CN) (2017JJA180826), Innovation Project of Guangxi Graduate Education (CN) (201601009) and Key Laboratory Open Project Fund of Guangxi Zhuang Autonomous Region (CN) (kfkt20160064). Conflict of Interest Statement The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Supplementary Material The Supplementary Material for this article can be fou...
Source: Frontiers in Physiology - April 23, 2019 Category: Physiology Source Type: research

Relevance of stromal interaction molecule 1 (STIM1) in experimental and human stroke
Pflugers Arch. 2021 Nov 10. doi: 10.1007/s00424-021-02636-w. Online ahead of print.ABSTRACTStroke represents a main cause of death and permanent disability worldwide. In the attempt to develop targeted preventive and therapeutic strategies, several efforts were performed over the last decades to identify the specific molecular abnormalities preceding cerebral ischemia and neuronal death. In this regard, mitochondrial dysfunction, autophagy, and intracellular calcium homeostasis appear important contributors to stroke development, as underscored by recent pre-clinical evidence. Intracellular calcium (Ca2+) homeostasis is re...
Source: Pflugers Archiv : European Journal of Physiology - November 10, 2021 Category: Physiology Authors: Rosita Stanzione Maurizio Forte Maria Cotugno Franca Bianchi Simona Marchitti Speranza Rubattu Source Type: research

Neuromuscular and Muscle Metabolic Functions in MELAS Before and After Resistance Training: A Case Study
Conclusion To conclude, this study suggests a preserved plasticity in the skeletal muscle of a patient with MELAS. More importantly, Resistance Training appears to be a safe and effective method to increase skeletal muscle function in this patient population, and this effect is mediated by both neuromuscular and mitochondrial adaptations. However, particular attention and caution is needed in the interpretation of the data of this single case study and further studies are warranted including larger sample of patients. Ethics Statement For this case study the participant caregiver provided written informed consent. Auth...
Source: Frontiers in Physiology - April 25, 2019 Category: Physiology Source Type: research

Iron Metabolism and Brain Development in Premature Infants
Yafeng Wang1,2,3, Yanan Wu2, Tao Li1,2,3, Xiaoyang Wang2,4 and Changlian Zhu2,3* 1Department of Neonatology (NICU), Children’s Hospital Affiliated Zhengzhou University, Zhengzhou, China 2Henan Key Laboratory of Child Brain Injury, Institute of Neuroscience and Third Affiliated Hospital of Zhengzhou University, Zhengzhou, China 3Department of Clinical Neuroscience, Center for Brain Repair and Rehabilitation, Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden 4Department of Physiology, Sahlgrenska Academy, Institute of Neuroscience and Physiology, University of Got...
Source: Frontiers in Physiology - April 24, 2019 Category: Physiology Source Type: research

Intratubular, Intracellular, and Mitochondrial Angiotensin II/AT1 (AT1a) Receptor/NHE3 Signaling Plays a Critical Role in Angiotensin II-Induced Hypertension and Kidney Injury
The objectives of this invited article are to review and discuss our recent findings that (a) circulating and intratubular Ang II is taken up by the proximal tubules via the (AT1) AT1a receptor-dependent mechanism, (b) intracellular administration of Ang II in proximal tubule cells or adenovirus-mediated overexpression of an intracellular Ang II fusion protein selectively in the mitochonria of the proximal tubules induces blood pressure responses, and (c) genetic deletion of AT1 (AT1a) receptors or the Na+/H+ exchanger 3 selectively in the proximal tubules decreases basal blood pressure and attenuates Ang II-induced hypert...
Source: Frontiers in Physiology - August 2, 2021 Category: Physiology Source Type: research

Long-term wheel running compromises diaphragm function but improves cardiac and plantarflexor function in the mdx mouse
Dystrophin-deficient muscles suffer from free radical injury, mitochondrial dysfunction, apoptosis, and inflammation, among other pathologies that contribute to muscle fiber injury and loss, leading to wheelchair confinement and death in the patient. For some time, it has been appreciated that endurance training has the potential to counter many of these contributing factors. Correspondingly, numerous investigations have shown improvements in limb muscle function following endurance training in mdx mice. However, the effect of long-term volitional wheel running on diaphragm and cardiac function is largely unknown. Our purp...
Source: Journal of Applied Physiology - September 1, 2013 Category: Physiology Authors: Selsby, J. T., Acosta, P., Sleeper, M. M., Barton, E. R., Sweeney, H. L. Tags: ARTICLES Source Type: research

Targeting Aldehyde Dehydrogenase 2: New Therapeutic Opportunities
A family of detoxifying enzymes called aldehyde dehydrogenases (ALDHs) has been a subject of recent interest, as its role in detoxifying aldehydes that accumulate through metabolism and to which we are exposed from the environment has been elucidated. Although the human genome has 19 ALDH genes, one ALDH emerges as a particularly important enzyme in a variety of human pathologies. This ALDH, ALDH2, is located in the mitochondrial matrix with much known about its role in ethanol metabolism. Less known is a new body of research to be discussed in this review, suggesting that ALDH2 dysfunction may contribute to a variety of h...
Source: Physiological Reviews - January 1, 2014 Category: Physiology Authors: Chen, C.-H., Ferreira, J. C. B., Gross, E. R., Mochly-Rosen, D. Tags: Articles Source Type: research

Targeting aldehyde dehydrogenase 2: new therapeutic opportunities.
Abstract A family of detoxifying enzymes called aldehyde dehydrogenases (ALDHs) has been a subject of recent interest, as its role in detoxifying aldehydes that accumulate through metabolism and to which we are exposed from the environment has been elucidated. Although the human genome has 19 ALDH genes, one ALDH emerges as a particularly important enzyme in a variety of human pathologies. This ALDH, ALDH2, is located in the mitochondrial matrix with much known about its role in ethanol metabolism. Less known is a new body of research to be discussed in this review, suggesting that ALDH2 dysfunction may contribute...
Source: Physiological Reviews - January 1, 2014 Category: Physiology Authors: Chen CH, Ferreira JC, Gross ER, Mochly-Rosen D Tags: Physiol Rev Source Type: research

Hypoxia and Ischemia-Reperfusion: A BiK Contribution?
Abstract Over the last decades, cardiovascular disease has become the primary cause of death in the Western world, and this trend is expanding throughout the world. In particular, atherosclerosis and the subsequent vessel obliterations are the primary cause of ischemic disease (stroke, coronary heart disease). Excess calcium influx into the cells is one of the major pathophysiological mechanisms important for ischemic injury in the brain and heart in humans. The large conductance calcium-activated K(+) channels (BK) are thus interesting candidates to protect against excess calcium influx and the events leading to ...
Source: American Journal of Physiology. Heart and Circulatory Physiology - July 11, 2014 Category: Physiology Authors: Tano JY, Gollasch M Tags: Am J Physiol Heart Circ Physiol Source Type: research

Ageing, metabolism and cardiovascular disease.
This article is protected by copyright. All rights reserved. PMID: 26391109 [PubMed - as supplied by publisher]
Source: The Journal of Physiology - September 22, 2015 Category: Physiology Authors: Costantino S, Paneni F, Cosentino F Tags: J Physiol Source Type: research

Ischemia/Reperfusion.
Authors: Kalogeris T, Baines CP, Krenz M, Korthuis RJ Abstract Ischemic disorders, such as myocardial infarction, stroke, and peripheral vascular disease, are the most common causes of debilitating disease and death in westernized cultures. The extent of tissue injury relates directly to the extent of blood flow reduction and to the length of the ischemic period, which influence the levels to which cellular ATP and intracellular pH are reduced. By impairing ATPase-dependent ion transport, ischemia causes intracellular and mitochondrial calcium levels to increase (calcium overload). Cell volume regulatory mechanisms...
Source: Comprehensive Physiology - February 1, 2017 Category: Physiology Tags: Compr Physiol Source Type: research

Oral N-acetylcysteine and exercise tolerance in mild chronic obstructive pulmonary disease
In conclusion, modulation of plasma redox status with oral NAC treatment was not translated into beneficial effects on central or peripheral components of the oxygen transport pathway, thereby failing to improve exercise tolerance in nonhypoxemic patients with mild COPD. NEW & NOTEWORTHY Acute antioxidant treatment with N-acetylcysteine (NAC) elevated plasma glutathione but did not modulate central or peripheral components of the O2 transport pathway, thereby failing to improve exercise tolerance in patients with mild chronic obstructive pulmonary disease (COPD).
Source: Journal of Applied Physiology - May 18, 2017 Category: Physiology Authors: Hirai, D. M., Jones, J. H., Zelt, J. T., da Silva, M. L., Bentley, R. F., Edgett, B. A., Gurd, B. J., Tschakovsky, M. E., ODonnell, D. E., Neder, J. A. Tags: RESEARCH ARTICLE Source Type: research

Neuronal Cell Death.
Abstract Neuronal cell death occurs extensively during development and pathology, where it is especially important because of the limited capacity of adult neurons to proliferate or be replaced. The concept of cell death used to be simple as there were just two or three types, so we just had to work out which type was involved in our particular pathology and then block it. However, we now know that there are at least a dozen ways for neurons to die, that blocking a particular mechanism of cell death may not prevent the cell from dying, and that non-neuronal cells also contribute to neuronal death. We review here t...
Source: Physiological Reviews - March 1, 2018 Category: Physiology Authors: Fricker M, Tolkovsky AM, Borutaite V, Coleman M, Brown GC Tags: Physiol Rev Source Type: research

Prenatal hypoxia impairs cardiac mitochondrial and ventricular function in guinea pig offspring in a sex-related manner.
CONCLUSION: Prenatal HPX is a programming stimulus that increases MAP and decreases cardiac and mitochondrial function in male offspring. Sex-related differences in the contractile and mitochondrial responses suggest female GPs are protected against cardiovascular programming of prenatal HPX. PMID: 30365351 [PubMed - as supplied by publisher]
Source: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology - October 26, 2018 Category: Physiology Authors: Thompson LP, Chen L, Polster BM, Pinkas G, Song H Tags: Am J Physiol Regul Integr Comp Physiol Source Type: research

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