Busca avançada
Ano de início
Entree
(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Increased Clearance of Reactive Aldehydes and Damaged Proteins in Hypertension-Induced Compensated Cardiac Hypertrophy: Impact of Exercise Training

Texto completo
Autor(es):
Campos, Juliane Cruz [1] ; Fernandes, Tiago [2] ; Grassmann Bechara, Luiz Roberto [1] ; da Paixao, Nathalie Alves [2] ; Brum, Patricia Chakur [2] ; de Oliveira, Edilamar Menezes [2] ; Batista Ferreira, Julio Cesar [1]
Número total de Autores: 7
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Anat, BR-05508000 Sao Paulo, SP - Brazil
[2] Univ Sao Paulo, Sch Phys Educ & Sport, BR-05508030 Sao Paulo, SP - Brazil
Número total de Afiliações: 2
Tipo de documento: Artigo Científico
Fonte: OXIDATIVE MEDICINE AND CELLULAR LONGEVITY; 2015.
Citações Web of Science: 16
Resumo

Background. We previously reported that exercise training (ET) facilitates the clearance of damaged proteins in heart failure. Here, we characterized the impact of ET on cardiac protein quality control during compensated ventricular hypertrophy in spontaneously hypertensive rats (SHR). Methods and Results. SHR were randomly assigned into sedentary and swimming-trained groups. Sedentary SHR displayed cardiac hypertrophy with preserved ventricular function compared to normotensive rats, characterizing a compensated cardiac hypertrophy. Hypertensive rats presented signs of cardiac oxidative stress, depicted by increased lipid peroxidation. However, these changes were not followed by accumulation of lipid peroxidation-generated reactive aldehydes and damaged proteins. This scenario was explained, at least in part, by the increased catalytic activity of both aldehyde dehydrogenase 2 (ALDH2) and proteasome. Of interest, ET exacerbated cardiac hypertrophy, improved ventricular function, induced resting bradycardia, and decreased blood pressure in SHR. These changes were accompanied by reduced cardiac oxidative stress and a consequent decrease in ALDH2 and proteasome activities, without affecting small chaperones levels and apoptosis in SHR. Conclusion. Increased cardiac ALDH2 and proteasomal activities counteract the deleterious effect of excessive oxidative stress in hypertension-induced compensated cardiac hypertrophy in rats. ET has a positive effect in reducing cardiac oxidative stress without affecting protein quality control. (AU)

Processo FAPESP: 06/56321-6 - Participação das isoformas proteína quinase C βII e proteína quinase C ε na insuficiência cardíaca induzida por infarto do miocárdio
Beneficiário:Julio Cesar Batista Ferreira
Linha de fomento: Bolsas no Brasil - Doutorado
Processo FAPESP: 12/05765-2 - Contribuição da enzima aldeído desidrogenase 2 na progressão da insuficiência cardíaca
Beneficiário:Julio Cesar Batista Ferreira
Linha de fomento: Auxílio à Pesquisa - Apoio a Jovens Pesquisadores