Adhesive hydrogels with tunable mechanical properties and strong adhesion to wet, dynamic tissues have emerged as promising materials for tissue repair, with potential applications in wound closure, hemorrhage control, and surgical adhesives. This review highlights the key design principles, material classifications, and recent advances in adhesive hydrogels designed for vascular repair. The limitations of existing adhesive hydrogels, including insufficient mechanical durability, suboptimal biocompatibility, and challenges in targeted delivery, are critically evaluated. Furthermore, innovative strategies—such as incorporating self-healing capabilities, developing stimuli-responsive systems, integrating functional nanocomposites, and employing advanced fabrication techniques like 3D bioprinting—are discussed to enhance adhesion, mechanical stability, and vascular tissue regeneration. While significant progress has been made, further research and optimization are necessary to advance these materials toward clinical translation, offering a versatile and minimally invasive alternative to traditional vascular repair techniques.

Endovascular procedures require sheaths with contradictory mechanical properties: flexibility for navigation through tortuous vessels, yet rigidity for device delivery. Current approaches rely on multiple device exchanges, increasing procedural time, and complication risks. Here we present a novel endovascular sheath design scheme with dynamically controllable flexural rigidity along its entire length. The device incorporates axially aligned metal string arrays between inner and outer lumens, enabling transition between flexible and rigid states through suction actuation. Three-point bend testing demonstrated that actuation increases flexural rigidity from the range associated with diagnostic catheters to that associated with support sheaths. In simulated contralateral access procedures, the device reduced access time to 1/3 of the time required when using conventional approaches. in vivo porcine studies validated the sheath's ability to navigate tortuous anatomy in its flexible state and successfully support advancement of increasingly rigid therapeutic devices when actuated. Technology enables single-sheath delivery of treatment, potentially reducing procedural complexity, decreasing complication rates, and improving patient outcomes across various endovascular interventions. This design represents a promising approach to combining catheter and sheath design that benefits both peripheral and neurovascular procedures.

BACKGROUND: Cept1 is essential for de novo phopholipogenesis and is impacted by diabetes. We previously demonstrated that conditional knockdown of Cept1 in the endothelium leads to reduced tissue recovery. Therefore, we hypothesized that Cept1 overexpression may also be sufficient in promoting postischemic angiogenesis and recovery in the setting of diabetes. METHODS: CEPT1 (choline-ethanolamine phosphotransferase 1) content was evaluated in the peripheral arteries of human patients with peripheral artery disease and with or without diabetes. We also engineered a conditional endothelial cell (EC)–specific Cept1 overexpression mouse ( Cept1 ^fl/fl Cre ⁺ ) in adult C57BL/6J (C57 black 6J) mice and performed unilateral hindlimb ischemia to assess the role of Cept1 in promoting angiogenesis. Murine aortae and ECs were harvested for single-cell RNA sequencing and molecular pathway analysis. RESULTS: In human arterial intima, CEPT1 was elevated in the setting of peripheral artery disease and diabetes, along with ACOX1 (acyl-coenzyme A oxidase 1), VEGF (vascular endothelial growth factor) R2, p-Akt (phosphorylated Akt), and p-eNOS (phosphorylated endothelial nitric oxide synthase). In mice, single-cell RNA sequencing demonstrated that ECs with Cept1 overexpression were enriched with wound healing, angiogenesis, sprouting, and cell migration pathways. Diabetic Cept1 ^fl/fl Cre ⁺ mice that underwent hindlimb ischemia demonstrated improved hindlimb perfusion and angiogenesis, and their aortic rings had increased ex vivo capillary sprouting. Cept1 overexpression in ECs significantly increased migration, tubule formation, and proliferation as predicted by single-cell RNA sequencing. Cept1 overexpression in ECs also led to increased expression of Pparα , Acox1 , Vegfa , and Vegfr2 . Similarly, treatment with si Ppar α and inhibitors for PPARα (peroxisome proliferator-activated receptor α; GW6471), VEGFR2 (ZM323881), Akt (LY294002), and eNOS (L-NAME [nitro-L-arginine methyl ester]) abrogated CEPT1-induced EC migration. CONCLUSIONS: Cept1 overexpression promotes EC function and postischemic recovery. The impact of CEPT1 on ECs is at least in part dependent on p-Akt/p-eNOS angiogenic signaling and PPARα. Because CEPT1 is elevated in diseased human peripheral arterial tissue, these findings suggest that CEPT1 may be playing an important compensatory role in vascular recovery and reperfusion following ischemic injury in the setting of diabetes.