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Roles of lipocalin 2 and adiponectin in iron overload cardiomyopathy
Natthaphat Siri-Angkul1,2,3, Siriporn C Chattipakorn1,3,4, Nipon Chattipakorn1,2,3
1Faculty of Medicine, Cardiac Electrophysiology Research and Training Center, Chiang Mai University, Chiang Mai, Thailand.
Insights
Thalassemia patients develop iron overload cardiomyopathy due to increased iron burden. This review explores lipocalin 2 and adiponectin
Area of Science:
- Cardiovascular Medicine
- Hematology
- Biochemistry
Background:
- Thalassemia, a common genetic disorder, leads to iron overload from ineffective erythropoiesis, hemolysis, and transfusions.
- Iron overload cardiomyopathy is a severe complication and leading cause of mortality in thalassemia patients.
- Key mechanisms involve cellular iron mishandling, chronic inflammation, and oxidative stress.
Purpose of the Study:
- To investigate the roles of lipocalin 2 and adiponectin in iron overload cardiomyopathy.
- To provide a comprehensive overview of current research on these molecules in thalassemia.
Main Methods:
- Comprehensive review of in vitro and in vivo studies.
- Analysis of clinical studies in thalassemia patients.
Main Results:
- Lipocalin 2, an iron-transporting protein, and adiponectin, an anti-inflammatory adipokine, show potential roles in iron overload cardiomyopathy.
- Summarizes findings from experimental and clinical investigations.
Conclusions:
- Lipocalin 2 and adiponectin are emergent molecules requiring further investigation in iron overload cardiomyopathy.
- Understanding their impact is crucial for managing cardiac complications in thalassemia.
Abstract:
Thalassemia is among the most common genetic diseases worldwide. Ineffective erythropoiesis, chronic hemolysis, and regular blood transfusion in thalassemia patients lead to increased iron burden. Iron overload cardiomyopathy is the most severe co-morbidity and most common cause of mortality in thalassemia patients. Although its associated mechanisms are still not completely understood, cellular iron mishandling, chronic inflammation, and oxidative stress appear to be the key processes involved. In order to acquire a more comprehensive insight of the impact of cardiac iron overload, these alterations need to be intensively investigated. This comprehensive mini-review focuses on two emergent molecules which have been shown to potentially play significant roles in iron overload cardiomyopathy. These two molecules are an iron-transporting protein, lipocalin 2, and an anti-inflammatory adipokine, adiponectin. Reports from in vitro and in vivo studies are comprehensively summarized. Clinical studies examining the roles of these molecules in thalassemia patients are also presented and discussed.
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