Catestatin improves heart metabolic flexibility by promoting mitochondrial structure and function Article Swipe
Avinash Dakshinamoorthy
,
Satadeepa Kal
,
Nilima Biswas
,
Sumana Mahata
,
Kechun Tang
,
Teresa Pasqua
,
Ennio Avolio
,
Suborno Jati
,
Gautam Bandyopadhyay
,
Brian P. Head
,
Hemal H. Patel
,
Geert van den Bogaart
,
Debashis Sahoo
,
Sanjib Senapati
,
Sushil K. Mahata
·
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1101/2024.12.29.630689
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1101/2024.12.29.630689
Hypertension, a major cause of cardiomyopathy, is one of the most critical risk factors for heart failure and mortality worldwide. Loss of metabolic flexibility of cardiomyocytes is one of the major causes of heart failure. Although Catestatin (CST) treatment is known to be both hypotensive and cardioprotective, its effect on cardiac metabolism is unknown. In this study, we undertook a transcriptomic approach to identify differentially expressed genes that were filtered using Boolean implication relationships to develop a model of gene regulation in saline or CST-supplemented CST knockout (CST-KO) mice. The analysis revealed a set of gene signatures (fibroblast, cardiomyocyte, and macrophage) rescued after CST supplemented CST-KO mice compared to wild-type. Furthermore, we independently validated these gene signature models using publicly available patient datasets. Since the gene signature includes genes related to glucose, fatty acid metabolism, and mitochondrial function, we assessed the glucose and fatty acid uptake after CST treatment. We found that CST treatment can restore the cardiac metabolic inflexibility in CST-KO heart due to the metabolic shift of glucose utilization to fatty acid as energy source. Binding studies after immunoprecipitation and mass spectrometry revealed CST binding with ATP synthase, supported by molecular simulation and computational modeling that predicted CST binding to α/β subunit of ATP synthase. Colocalization of CST with mitochondria and increased mitochondrial membrane potential and ATP production upon CST treatment in neonatal cardiomyocytes further exhibit CST as a key regulator of cardiac metabolism and mitochondrial function.
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- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1101/2024.12.29.630689
- OA Status
- green
- References
- 82
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4405895870
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https://doi.org/10.1101/2024.12.29.630689Digital Object Identifier
- Title
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Catestatin improves heart metabolic flexibility by promoting mitochondrial structure and functionWork title
- Type
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preprintOpenAlex work type
- Language
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enPrimary language
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2024Year of publication
- Publication date
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2024-12-30Full publication date if available
- Authors
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Avinash Dakshinamoorthy, Satadeepa Kal, Nilima Biswas, Sumana Mahata, Kechun Tang, Teresa Pasqua, Ennio Avolio, Suborno Jati, Gautam Bandyopadhyay, Brian P. Head, Hemal H. Patel, Geert van den Bogaart, Debashis Sahoo, Sanjib Senapati, Sushil K. MahataList of authors in order
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https://doi.org/10.1101/2024.12.29.630689Publisher landing page
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YesWhether a free full text is available
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greenOpen access status per OpenAlex
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https://www.ncbi.nlm.nih.gov/pmc/articles/11722442Direct OA link when available
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Flexibility (engineering), Function (biology), Business, Chemistry, Cell biology, Biology, Economics, ManagementTop concepts (fields/topics) attached by OpenAlex
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0Total citation count in OpenAlex
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10Other works algorithmically related by OpenAlex
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