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Editorial
. 2024 Apr 23;149(17):1372-1374.
doi: 10.1161/CIRCULATIONAHA.124.068738. Epub 2024 Apr 22.

Mediating Metabolism: Inhibition of Malic Enzyme 1 (ME1) Restores Endothelial Bioenergetics and Adenosine Signaling in Pulmonary Hypertension

Rashmi J Rao  1 , Stephen Y Chan  1
Affiliations
Editorial

Mediating Metabolism: Inhibition of Malic Enzyme 1 (ME1) Restores Endothelial Bioenergetics and Adenosine Signaling in Pulmonary Hypertension

Rashmi J Rao et al. Circulation. .
No abstract available

Keywords: Editorials; adenosine; energy metabolism; hypertension, pulmonary; malate dehydrogenase (decarboxylating).

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Conflict of interest statement

Disclosures Dr Chan has served as a consultant for Merck, Janssen, and United Therapeutics. Dr Chan is a director, officer, and shareholder in Synhale Therapeutics; has held grants from United Therapeutics, Bayer, and the WoodNext Foundation; and has filed patent applications for metabolism and next-generation therapeutics in PH. R.J. Rao reports no conflicts.

Figures

Figure 1:
Figure 1:. A role for malic enzyme 1 (ME1) in pulmonary hypertension.
ME1 inhibition promotes ATP-dependent adenosine biosynthesis by maintaining the balance between mitochondrial oxidative phosphorylation and cytosolic glycolysis. This leads to enhanced downstream adenosine signaling, found to ameliorate PH in vivo. Future studies are necessary to further define cell-type interactions and the role of ME1 in cellular metabolic networks, as well as diagnostic and therapeutic applications of these findings. Diagram generated via biorender.com.
See this image and copyright information in PMC

Comment on

References

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