The effect of hypoxia and reoxygenation in the response of mesangial cells to angiotensin II in vitro

Razvickas, Clara Versolato; Borges, Fernanda Teixeira; Oliveira, Andréia Silva de; Schor, Nestor; Boim, Mirian Aparecida

doi:10.5935/0101-2800.20130044

Cited by 2 publications

(2 citation statements)

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“…There is a compensatory increase in Na + /Ca 2+ exchange as an adaptation for high internal Na + caused when Na + /K + pumping is impaired during ischaemia, and the Na + /K + exchanger is increased during reperfusion (Hoffman et al 2004). ROS and high cytosolic [Ca 2+ ] then trigger mitochondrial permeability transition pore opening and myofibrillar hypercontractility as pH rises (Razvickas et al 2013). In addition, cardiac ischaemia also down-regulates HSP70, SOD, catalase and glutathione peroxidase in skeletal muscle (Lawler et al 2006a), thus reducing cardioprotection.…”

Section: Exercise Preconditioning and Ischaemia-reperfusionmentioning

confidence: 99%

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Mitochondria in the middle: exercise preconditioning protection of striated muscle

Lawler¹,

Rodriguez²,

Hord³

2016

The Journal of Physiology

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Cellular and physiological adaptations to an atmosphere which became enriched in molecular oxygen spurred the development of a layered system of stress protection, including antioxidant and stress response proteins. At physiological levels reactive oxygen and nitrogen species regulate cell signalling as well as intracellular and intercellular communication. Exercise and physical activity confer a variety of stressors on skeletal muscle and the cardiovascular system: mechanical, metabolic, oxidative. Transient increases of stressors during acute bouts of exercise or exercise training stimulate enhancement of cellular stress protection against future insults of oxidative, metabolic and mechanical stressors that could induce injury or disease. This phenomenon has been termed both hormesis and exercise preconditioning (EPC). EPC stimulates transcription factors such as Nrf‐1 and heat shock factor‐1 and up‐regulates gene expression of a cadre of cytosolic (e.g. glutathione peroxidase and heat shock proteins) and mitochondrial adaptive or stress proteins (e.g. manganese superoxide dismutase, mitochondrial KATP channels and peroxisome proliferator activated receptor γ coactivator‐1 (PGC‐1)). Stress response and antioxidant enzyme inducibility with exercise lead to protection against striated muscle damage, oxidative stress and injury. EPC may indeed provide significant clinical protection against ischaemia–reperfusion injury, Type II diabetes and ageing. New molecular mechanisms of protection, such as δ‐opioid receptor regulation and mitophagy, reinforce the notion that mitochondrial adaptations (e.g. heat shock proteins, antioxidant enzymes and sirtuin‐1/PGC‐1 signalling) are central to the protective effects of exercise preconditioning.

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Section: Exercise Preconditioning and Ischaemia-reperfusionmentioning

confidence: 99%

“…ROS and high cytosolic [Ca 2+ ] then trigger mitochondrial permeability transition pore opening and myofibrillar hypercontractility as pH rises (Razvickas et al . ). In addition, cardiac ischaemia also down‐regulates HSP70, SOD, catalase and glutathione peroxidase in skeletal muscle (Lawler et al .…”

Section: Introductionmentioning

confidence: 97%