Exercise training contributes to H2O2/VEGF signaling in the lung of rats with monocrotaline-induced pulmonary hypertension

Colombo, Rafael; Siqueira, Rafaela; Conzatti, Adriana; Seolin, Bruna Gazzi de Lima; Fernandes, Tania Regina Gattelli; Godoy, Alessandra Eifler Guerra; Litvin, Isnard Elman; Silva, Jairo Montemor Augusto; Tucci, Paulo José Ferreira; Araújo, Alex Sander da Rosa; Belló‐Klein, Adriane

doi:10.1016/j.vph.2016.06.006

Cited by 25 publications

(23 citation statements)

References 34 publications

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“…However, clinical evidence in support of ET use in PAH is growing, thus requiring an effort to elucidate the benefits of ET in these patients. A recent study has focused on the role of H 2 O 2 -induced angiogenesis as a possible mechanism to explain the increased pulmonary vascular reserve during exercise (42). It has been demonstrated an increase of H 2 O 2 in PAH-trained animals (42).…”

Section: Efficacy Of Training In Pah On Functional Capacity Qol Surmentioning

confidence: 99%

“…A recent study has focused on the role of H 2 O 2 -induced angiogenesis as a possible mechanism to explain the increased pulmonary vascular reserve during exercise (42). It has been demonstrated an increase of H 2 O 2 in PAH-trained animals (42). Aerobic ET also facilitated the expression of VEGF gene, and its positive correlation with Akt phosphorylation.…”

Section: Efficacy Of Training In Pah On Functional Capacity Qol Surmentioning

confidence: 99%

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Exercise training in pulmonary arterial hypertension

Vecchia

Bussotti

2018

J. Thorac. Dis.

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Pulmonary arterial hypertension (PAH) is characterized by a continuous increase in pre-capillary pulmonary vascular resistance (PVR) with a progressive reduction of cardiac output (CO). Similar to what occurs in left heart failure (HF), this represents the initial phase of a syndrome characterized by the progressive development of dyspnea and fatigue with increasing deterioration of exercise tolerance. Although the therapies introduced in the last two decades have determined a significant improvement of the clinical conditions of PAH patients, they have a little impact on exercise capacity and prognosis. However, as previously demonstrated for HF, recent pilot studies have reported that physical and respiratory rehabilitation may have a specific role in the management of PAH. Despite potential risks, so far all studies agree that exercise training (ET) improves exercise capacity, quality of life (QoL), muscle function and pulmonary circulation. We will review the pathophysiological mechanisms underlying the functional incompetence of PAH patients, the effects of ET on clinical and functional parameters, the selection criteria for inclusion of patients in a training program, the suggested monitoring of beneficial effects or possible side effects induced by ET. Finally, we discuss of the possible exercise induced amelioration of prognosis in PAH.

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Section: Efficacy Of Training In Pah On Functional Capacity Qol Surmentioning

confidence: 99%

Section: Efficacy Of Training In Pah On Functional Capacity Qol Surmentioning

confidence: 99%

Exercise training in pulmonary arterial hypertension

Vecchia

Bussotti

2018

J. Thorac. Dis.

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“…In the majority of the studies, exercise training showed beneficial effects on cardiac remodelling [34,[36][37][38][40][41][42][43][44][45][46]48]. Still, others reported no improvement [47,49] or aggravation [50].…”

Section: Cardiac Adaptationsmentioning

confidence: 99%

“…The impact of exercise training on pulmonary vasculature remains inconclusive, with experimental studies showing improvement [34,37,41,42,45], no improvement [40,43,44,46,48,49] or aggravation [50]. However, only five studies explored the molecular mechanisms associated with exercise training effects.…”

Section: Pulmonary Adaptationsmentioning

confidence: 99%

Mechanisms underlying the impact of exercise training in pulmonary arterial hypertension

Nogueira-Ferreira

Moreira-Gonçalves

Santos

et al. 2018

Respiratory Medicine

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Pulmonary arterial hypertension (PAH) is a devastating disease characterized by progressive increases in pulmonary vascular resistance that can ultimately lead to right ventricle failure and death. Common symptoms include shortness of breath, fatigue, dizziness and chest pain, which negatively impact the functional capacity and quality of life. Despite the improvements in disease-targeted therapies, PAH remains incurable and with a high mortality rate, requiring effective therapeutic strategies. Exercise training is an important adjunct non-pharmacological treatment for patients with left heart failure and chronic obstructive pulmonary disease. Although exercise training was discouraged in PAH because of safety concerns, recent studies support that supervised exercise training is safe and beneficial in patients with stable PAH. However, the molecular mechanisms underlying these improvements are still poorly understood. This review summarizes and integrates the emerging clinical and experimental studies describing the molecular alterations related with exercise training in PAH.

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“…24 Colombo et al reported that 5 weeks of aerobic exercise training on a treadmill, increased the levels of VEGF in lung tissue of rats. 25 While Krenc et al' study showed that after a long period of aerobic exercises training, reducing VEGF levels observed. 26 So, given the importance of prevention of lung cancer, and also the lack of necessary and adequate information regarding the impact of exercise on annexin A2 and VEGF levels in lung's tissue exposed to NNK, the aim of this study was to examine the effects of submaximal swimming training on annexin A2 and VEGF in Wistar rats exposed to NNK.…”

mentioning

confidence: 95%

Modulation of Vascular Endothelial Growth Factor and Annexin A2 in Response to 4-(Methylnitrosamino)-1-(3-pyridyl)-1-Butanone -Induced Inflammation via Swimming Training

Barzegari

Mirdar

Ranayi

2018

IJAAI

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The nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK; nicotine derived nitrosamine ketone) is one of the strongest carcinogens in tobacco which is involved in induction of lung cancer by changing the stimulation of vascular endothelial growth factor (VEGF) and annexin A2 expression. The aim of this study was to investigate the changes in resting levels of annexin A2 and VEGF in lung tissues of rats exposed NNK after 12 weeks of aerobic submaximal swimming training. For this purpose, 46 Wistar rats were randomly divided into five groups consist of training, training + NNK, NNK, saline and control. NNK-induced groups received NNK subcutaneously one day per week at a rate of 12/5 mg per kg body weight and the training groups performed submaximal swimming training for 12 weeks. The levels of VEGF and annexin A2 in lung tissue were measured respectively by ELISA and immunohistochemistry. To analyze the data; ANOVA and Tukey's test were used at a significance level of p<0.05. Findings indicated that 12 weeks submaximal swimming training decreased the levels of VEGF and annexin A2 in lung tissue significantly when compared to NNK group (p<0.001). There was no significant correlation between VEGF and annexin A2 levels in all study groups (p≥0.05). Generally, it could be confirmed that regular submaximal aerobic training plays an important role in inhibition of the effects of lung inflammation induced by NNK via decreased levels of VEGF and annexin A2.

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Exercise training contributes to H2O2/VEGF signaling in the lung of rats with monocrotaline-induced pulmonary hypertension

Cited by 25 publications

References 34 publications

Exercise training in pulmonary arterial hypertension

Exercise training in pulmonary arterial hypertension

Mechanisms underlying the impact of exercise training in pulmonary arterial hypertension

Modulation of Vascular Endothelial Growth Factor and Annexin A2 in Response to 4-(Methylnitrosamino)-1-(3-pyridyl)-1-Butanone -Induced Inflammation via Swimming Training

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