Key result
Phylogenetic analysis links conserved calcium-handling proteins to diabetic cardiomyopathy pathogenesis.
This bioinformatic analysis highlights the potential central role of deranged calcium homeostasis and contractile protein impairment in the development of diabetic cardiomyopathy.
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Suggests calcium-handling proteins as targets in diabetic cardiomyopathy; hypothesis-generating and should not yet change practice.
Diabetic cardiomyopathy is a distinct clinical entity that produces asymptomatic heart failure in diabetic patients without evidence of coronary artery disease and hypertension. Abnormalities in diabetic cardiomyopathy include: myocardial hypertrophy, impairment of contractile proteins, accumulation of extracellular matrix proteins, formation of advanced glycation end products, and decreased left ventricular compliance. These abnormalities lead to the most common clinical presentation of diabetic cardiomyopathy in the form of diastolic dysfunction. We evaluated the role of various proteins that are likely to be involved in diabetic cardiomyopathy by employing multiple sequence alignment using ClustalW tool and constructed a Phylogenetic tree using functional protein sequences extracted from NCBI. Phylogenetic tree was constructed using Neighbour—Joining Algorithm in bioinformatics approach. These results suggest a causal relationship between altered calcium homeostasis and diabetic cardiomyopathy that implies that efforts directed to normalize calcium homeostasis could form a novel therapeutic approach.
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Rao et al. (2008) studied Diabetic cardiomyopathy. Bioinformatics phylogenetic analysis was evaluated on Phylogenetic distance between protein sequences. Phylogenetic analysis identified Na+-Ca2+-exchanger, protein kinase C-β, and Na+-K+-ATPase as having minimum distance, highlighting the role of altered calcium homeostasis in diabetic cardiomyopathy.
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