Leading-edge regenerative medicine can take advantage of improved knowledge of key roles played, both in stem cell fate determination and in cell growth/differentiation, by mechano-transduction and other physicochemical stimuli from the tissue environment. This prompted advanced nanomaterials research to provide tissue engineers with next-generation scaffolds consisting of smart nanocomposites and/or hydrogels with nanofillers, where balanced combinations of specific matrices and nanomaterials can mediate and finely tune such stimuli and cues. In this review, we focus on graphene-based nanomaterials as, in addition to modulating nanotopography, elastic modulus and viscoelastic features of the scaffold, they can also regulate its conductivity. This feature is crucial to the determination and differentiation of some cell lineages and is of special interest to neural regenerative medicine. Hereafter we depict relevant properties of such nanofillers, illustrate how problems related to their eventual cytotoxicity are solved via enhanced synthesis, purification and derivatization protocols, and finally provide examples of successful applications in regenerative medicine on a number of tissues.

Homo- and heterophilic binding mediated by the immunoglobulin (Ig)-like repeats of cell adhesion molecules play a pivotal role in cell-cell and cell-extracellular matrix interactions. L1CAM is crucial to neuronal differentiation, in both mature and developing nervous systems, and several studies suggest that its functional interactions are mainly mediated by Ig2–Ig2 binding. X-linked mutations in the human L1CAM gene are summarized as L1 diseases, including the most diagnosed CRASH neurodevelopmental syndrome. In silico simulations provided a molecular rationale for CRASH phenotypes resulting from mutations I179S and R184Q in the homophilic binding region of Ig2. A synthetic peptide reproducing such region could both mimic the neuritogenic capacity of L1CAM and rescue neuritogenesis in a cellular model of the CRASH syndrome, where the full L1CAM ectodomain proved ineffective. Presented functional evidence opens the route to the use of L1CAM-derived peptides as biotechnological and therapeutic tools.