**5. Conclusion**

Depending on the relative abundance and localization of the components of the cAMP signal‐ ling pathways, cAMP effects on VSMC vary in differentiated and trans-differentiated VSMCs (Figure 4). Because trans-differentiated VSMCs play a crucial role in atherosclerosis and are solely responsible for post-angioplasty restenosis, understanding molecular mechanisms leading to VSMC trans-differentiation is crucial to develop novel therapeutic strategies. Re‐ ducing post-angioplasty restenosis which affects 20-25% of patients treated with bare metal stents, is one of the major challenges in cardiovascular medicine. At the beginning of 2000's, the apparition of stents locally releasing anti-proliferative drugs (ie drug-eluting stents (DES), have significantly changed interventional cardiology, due to their remarkable ability to reduce restenosis compared to bare metal stents, However, their overwhelming success has quickly decreased since is limited due to an increased risk of late stent thrombosis. Poor re-endothelial‐ ization remains the major important pathologic predictor of late stent thrombosis [117], there‐ fore, it has been suggested that DES should ideally have a selective anti-migratory and/or proliferative effect on VSMCs, without affecting, or, even better, promoting re-endothelializa‐ tion [77,118]. Identifying the specific components of the cAMP pathway specifically involved in VSMC trans-differentiation may be a novel concept for the development of new drugs for DES, therefore improving the treatment of pathological vascular remodellings.

**Author details**

Martine Glorian\*

**References**

and Isabelle Limon

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\*Address all correspondence to: martine.glorian@snv.jussieu.fr

UR, Vieillissement, Stress et Inflammation, Université Pierre et Marie Curie, Paris, France

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**Figure 4.** Expression of cAMP components in differentiated and trans-differentiated VSMC and consequences on VSMC functions. AC adenylyl cyclase; AKAP A-kinase anchoring proteins; Epac exchange proteins directly activated by cAMP; CREB cAMP response element binding protein; PDE phosphodiesterases.
