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Journals / Turkish Journal of Medical Sciences / 2015 / Cilt: 45 - Sayı: 1

Stress-responsive factor regulation in patients suffering from type 2 diabetes and myocardial infarction

Sobia MUSHTAQ
Tahir ALI
Farhana ALTAF
Muhammad ABDULLAH
İram MURTAZA
Pages
148–152
Publication Date
2015-03-15
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: These findings suggest a possible link between decreased antioxidant (SOD) and increased ROS levels as well as calpain-1 expression, supporting the role of oxidative stress-regulatory factors in diabetes and myocardial infraction.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Pro-free radical oxidative stresses, as well as regulatory factors, are believed to be the key players in the development of diabetes and heart-related disorders such as myocardial infarction.
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Key Findings & Data:The aim of the present study was to highlight the role of oxidative stress-responsive factors (reactive oxygen species [ROS], super oxide dismutase [SOD], and calpain-1) in type 2 diabetes and myocardial infarction.
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Conclusion & Impact:Conclusion: These findings suggest a possible link between decreased antioxidant (SOD) and increased ROS levels as well as calpain-1 expression, supporting the role of oxidative stress-regulatory factors in diabetes and myocardial infraction.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Diabetes mellitus · myocardial infraction · super oxide dismutase

Abstract

Pro-free radical oxidative stresses, as well as regulatory factors, are believed to be the key players in the development of diabetes and heart-related disorders such as myocardial infarction. The aim of the present study was to highlight the role of oxidative stress-responsive factors (reactive oxygen species [ROS], super oxide dismutase [SOD], and calpain-1) in type 2 diabetes and myocardial infarction. Materials and methods: A total of 100 type 2 diabetes patients with myocardial infarction and 50 normal individuals were selected for this analysis. The levels of ROS and activities of SOD in the serum were determined. Serum calpain-1 expression was checked using western blotting. Results: The serum level of ROS and the expression of calpain-1 were significantly higher while the activity of SOD was significantly lower in diabetic patients with myocardial infraction compared to normal individuals. Conclusion: These findings suggest a possible link between decreased antioxidant (SOD) and increased ROS levels as well as calpain-1 expression, supporting the role of oxidative stress-regulatory factors in diabetes and myocardial infraction.

Özet

Pro-free radical oxidative stresses, as well as regulatory factors, are believed to be the key players in the development of diabetes and heart-related disorders such as myocardial infarction. The aim of the present study was to highlight the role of oxidative stress-responsive factors (reactive oxygen species [ROS], super oxide dismutase [SOD], and calpain-1) in type 2 diabetes and myocardial infarction. Materials and methods: A total of 100 type 2 diabetes patients with myocardial infarction and 50 normal individuals were selected for this analysis. The levels of ROS and activities of SOD in the serum were determined. Serum calpain-1 expression was checked using western blotting. Results: The serum level of ROS and the expression of calpain-1 were significantly higher while the activity of SOD was significantly lower in diabetic patients with myocardial infraction compared to normal individuals. Conclusion: These findings suggest a possible link between decreased antioxidant (SOD) and increased ROS levels as well as calpain-1 expression, supporting the role of oxidative stress-regulatory factors in diabetes and myocardial infraction.

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Cite This Article

MUSHTAQ, S., ALI, T., ALTAF, F., ABDULLAH, M., MURTAZA, İ. (2015). Stress-responsive factor regulation in patients suffering from type 2 diabetes and myocardial infarction. Turkish Journal of Medical Sciences, Cilt: 45 - Sayı: 1, 148–152. https://ajindex.com/articles/209660

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