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Angiogenic factor induced by ER stress promotes tissue repair after myocardial infarction

Myocardial infarction causes endoplasmic reticulum (ER) stress, thereby triggering the release of a set of poorly defined growth factors. A study shows that the growth factor CRELD2 is secreted in response to ER stress and is required for preserving heart function after myocardial infarction in mice.

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Fig. 1: Secreted CRELD2 promotes angiogenesis and infarct repair.


  1. Oh-hashi, K., Kunieda, R., Hirata, Y. & Kiuchi, K. Biosynthesis and secretion of mouse cysteine-rich with EGF-like domains 2. FEBS Lett. 585, 2481–2487 (2011). This paper shows that CRELD2 residing inside the ER might be secreted.

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  2. Kern, P. et al. Creld2 function during unfolded protein response is essential for liver metabolism homeostasis. FASEB J. 35, e21939 (2021). This paper describes Creld2-deficient mice.

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This is a summary of: Wu, X. et al. Cysteine-rich with EGF-like domains 2 (CRELD2) is an endoplasmic reticulum stress-inducible angiogenic growth factor promoting ischemic heart repair. Nat. Cardiovas. Res. (2024).

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Angiogenic factor induced by ER stress promotes tissue repair after myocardial infarction. Nat Cardiovasc Res 3, 108–109 (2024).

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