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Cardiac metabolism

Bile acids for diabetic cardiomyopathy

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Diabetes can cause heart failure by a toxic accumulation of lipids in cardiac myocytes, which impairs their function. This work shows that stimulation of the bile acid receptor TGR5 limits fatty acid uptake into cardiac myocytes and prevents the development of diabetic cardiomyopathy.

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Fig. 1: Impact of TGR5 activation and deletion on cardiac fatty acid metabolism in diabetic cardiomyopathy (DbCM).

References

  1. Maack, C. et al. Eur. Heart J. 39, 4243–4254 (2018).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  2. Seferović, P. M. & Paulus, W. J. Eur Heart J. 36, 1718–1727 (2015).

    Article  PubMed  Google Scholar 

  3. Wang, H. et al. Nat. Metab. https://doi.org/10.1038/s42255-024-01036-5 (2024).

  4. Jia, G., Hill, M. A. & Sowers, J. R. Circ. Res. 122, 624–638 (2018).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  5. Vaduganathan, M. et al. Lancet 400, 757–767 (2022).

    Article  CAS  PubMed  Google Scholar 

  6. Kosiborod, M. N. et al. N. Engl. J. Med. 389, 1069–1084 (2023).

    Article  CAS  PubMed  Google Scholar 

  7. Bertero, E. & Maack, C. Nat. Rev. Cardiol. 15, 457–470 (2018).

    Article  CAS  PubMed  Google Scholar 

  8. Zhang, X., Fan, J., Li, H., Chen, C. & Wang, Y. Aging Dis. 12, 826–840 (2021).

    Article  PubMed  PubMed Central  Google Scholar 

  9. Guo, C., Chen, W. D. & Wang, Y. D. Front. Physiol. 7, 646 (2016).

    PubMed  PubMed Central  Google Scholar 

  10. Mantovani, A. et al. Metabolites 11, 453 (2021).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  11. Chen, C. et al. J. Pharm. Biomed. Anal. 131, 473–481 (2016).

    Article  CAS  PubMed  Google Scholar 

  12. Wang, J. et al. J. Mol. Cell. Cardiol. 151, 3–14 (2021).

    Article  CAS  PubMed  Google Scholar 

  13. Eblimit, Z. et al. Cardiovasc. Ther. 36, e12462 (2018).

    Article  PubMed  Google Scholar 

  14. Lakić, B. et al. J. Diabetes Res. 2024, 4187796 (2024).

    Article  PubMed  PubMed Central  Google Scholar 

  15. Maack, C. et al. Eur. Heart J. 40, 3626–3644 (2019).

    Article  CAS  PubMed  Google Scholar 

Download references

Acknowledgements

Christoph Maack is funded by the Deutsche Forschungsgemeinschaft (DFG; Ma 2528/8–1, SFB 1525 — project no. 453989101), the German Center for Cardiovascular Research (DZHK) (EX-22) and the COST Action CA22169 (EU-METAHEART).

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Authors and Affiliations

  1. Department of Translational Research, Comprehensive Heart Failure Center, University Hospital Würzburg, Würzburg, Germany

    David Weissman & Christoph Maack

  2. Medical Clinic I, University Hospital Würzburg, Würzburg, Germany

    Christoph Maack

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  1. David Weissman
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  2. Christoph Maack
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Correspondence to Christoph Maack.

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Competing interests

C.M. is an advisor to Amgen, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Novo Nordisk and Servier, and received speaker honoraria from AstraZeneca, Bayer, Bristol Myers Squibb, Boehringer Ingelheim, Berlin Chemie, Edwards, Novartis, Novo Nordisk and Servier. D.W. declares no competing interests.

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Weissman, D., Maack, C. Bile acids for diabetic cardiomyopathy. Nat Metab (2024). https://doi.org/10.1038/s42255-024-01032-9

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