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Editorial
. 2024 Sep 13;135(7):774-776.
doi: 10.1161/CIRCRESAHA.124.325132. Epub 2024 Sep 12.

Cyclophilin(g) a Knowledge Gap in Heart Failure Pathogenesis

Marion Delaunay  1 , Zegeye H Jebessa  1 , Timothy A McKinsey  1
Affiliations
Editorial

Cyclophilin(g) a Knowledge Gap in Heart Failure Pathogenesis

Marion Delaunay et al. Circ Res. .
No abstract available

Keywords: Editorials; heart failure; isomerism; myocardial infarction; ventricular remodeling.

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Conflict of interest statement

T.A. McKinsey is a cofounder of Myracle Therapeutics, is on the scientific advisory boards of Eikonizo Therapeutics and Revier Therapeutics, received funding from Italfarmaco for an unrelated project, and has a subcontract from Eikonizo Therapeutics for an Small Business Innovation Research grant from the National Institutes of Health (HL154959). The other authors report no conflicts.

Figures

Figure.
Figure.. A model for regulation of pathological cardiac remodeling by extracellular CyPA.
Pathological stress in the heart results in increased expression of CyPA and release of extracellular CyPA (eCyPA) from cells. Binding to eCyPA to the EMMPRIN/CD147 receptor on cardiomyocytes stimulates ERK and possibly other signaling cascades, resulting in hypertrophy and stiffening of the cells. It is unknown whether cardiomyocytes that are stimulated with eCyPA activate cardiac fibroblasts and inflammatory cells through paracrine mechanisms, or if eCyPA directly engages these other cell types. The constellation of cardiomyocyte hypertrophy/stiffening, inflammation and fibrosis caused by eCyPA results in cardiac dysfunction and contributes to heart failure pathogenesis. Parts of this figure were made using BioRender.
See this image and copyright information in PMC

Comment on

References

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