2021
DOI: 10.1007/s10517-021-05272-7
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Expression of Bax and Bcl-2 Proteins in Left-Ventricular Cardiomyocytes in Wistar-Kyoto and SHR Rats with Insulin-Dependent Diabetes Mellitus

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Cited by 5 publications
(4 citation statements)
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“…This fact indicates that the activation of these proteins plays a maladaptive role in the activity of CMCs, which can serve as an important marker for assessing the progression of vascular damage in this type of pathology. A decrease in the expression of the HSP60/HSP10 complex relative to Bax was also found in all the pathological models studied, while this difference was less pronounced in the combined hypertension with DM group (43,98,143). Thus, a decrease in the production of HSP60 can be considered as one of the pathophysiological mechanisms of LV myocardial damage caused by hypertension and/or DM.…”
Section: The Role Of Hsps In Regulated Cell Deathmentioning
confidence: 75%
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“…This fact indicates that the activation of these proteins plays a maladaptive role in the activity of CMCs, which can serve as an important marker for assessing the progression of vascular damage in this type of pathology. A decrease in the expression of the HSP60/HSP10 complex relative to Bax was also found in all the pathological models studied, while this difference was less pronounced in the combined hypertension with DM group (43,98,143). Thus, a decrease in the production of HSP60 can be considered as one of the pathophysiological mechanisms of LV myocardial damage caused by hypertension and/or DM.…”
Section: The Role Of Hsps In Regulated Cell Deathmentioning
confidence: 75%
“…The level of Bcl-2 was also significantly increased and the Bcl-2/Bax ratio tended to increase, but remained below the control. This indicates a decrease of the apoptotic cascade in the comorbid pathology compared to isolated hypertension and DM ( 142 , 143 ).…”
Section: The Role Of Hsps In Regulated Cell Deathmentioning
confidence: 92%
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“…Interestingly, these functional alterations appear before the occurrence of morphological changes in the structure of the myocardium and microvasculature [ 112 ]. Subsequently, the activation of pro-apoptotic pathways determines the depletion of contractile myocardium which is replaced by fibrotic tissue [ 114 ], resulting in LV systo-diastolic dysfunction [ 116 ]. Moreover, chronic hyperglycemia triggers secondary pulmonary hypertension which contributes to RV hypertrophy and late systolic dysfunction (12 weeks from disease induction) [ 115 ].…”
Section: Drug Toxicity Modelsmentioning
confidence: 99%