There is increasing interest in the study of chiral degrees of freedom occurring in matter and in electromagnetic fields. Opportunities in quantum sciences will likely exploit two main areas that are the focus of this Review: (1) recent observations of the chiral-induced spin selectivity (CISS) effect in chiral molecules and engineered nanomaterials and (2) rapidly evolving nanophotonic strategies designed to amplify chiral light–matter interactions. On the one hand, the CISS effect underpins the observation that charge transport through nanoscopic chiral structures favors a particular electronic spin orientation, resulting in large room-temperature spin polarizations. Observations of the CISS effect suggest opportunities for spin control and for the design and fabrication of room-temperature quantum devices from the bottom up, with atomic-scale precision and molecular modularity. On the other hand, chiral–optical effects that depend on both spin- and orbital-angular momentum of photons could offer key advantages in all-optical and quantum information technologies. In particular, amplification of these chiral light–matter interactions using rationally designed plasmonic and dielectric nanomaterials provide approaches to manipulate light intensity, polarization, and phase in confined nanoscale geometries. Any technology that relies on optimal charge transport, or optical control and readout, including quantum devices for logic, sensing, and storage, may benefit from chiral quantum properties. These properties can be theoretically and experimentally investigated from a quantum information perspective, which has not yet been fully developed. There are uncharted implications for the quantum sciences once chiral couplings can be engineered to control the storage, transduction, and manipulation of quantum information. This forward-looking Review provides a survey of the experimental and theoretical fundamentals of chiral-influenced quantum effects and presents a vision for their possible future roles in enabling room-temperature quantum technologies.

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Vein graft failure limits the long-term patency of the saphenous vein used as a conduit for coronary artery bypass graft. Early graft adaptation involves some degree of intima hyperplasia to sustain the hemodynamic stress, but the progress to occlusion in some veins remains unclear. We have demonstrated that stretch-induced up-regulation of cysteine and glycine-rich protein 3 (Crp3) in rat jugular vein and human saphenous vein in response to arterialization. Here, we developed a Crp3-KO rat to investigate the role of Crp3 in vascular remodeling. After 28 days jugular vein arterialization, the intima layer was 3-fold thicker in the Crp3-KO that showed comparable smooth muscle cells (SMC) proliferation but an absence of early apoptosis observed in the wild-type rat (WT). We then investigated the role of Crp3 in early integrin-mediated signaling apoptosis in isolated jugular SMC. Interestingly, under basal conditions, ceramide treatment failed to induce apoptosis in both WT and Crp3-KO SMC. Under stretch, Crp3 expression increased in WT SMC and ceramide induced apoptosis. Immunoblotting analysis indicated that ceramide stretch-induced apoptosis in SMC is accompanied by a decrease in the phosphorylation status of both Fak and Akt, leading to an increase in Bax expression and caspase-3 cleavage. In contrast, ceramide failed to decrease Fak and Akt phosphorylation in Crp3-KO SMC and, therefore, there was no downstream induction of Bax expression and effector caspase-3 cleavage. Taken together, we provide evidence that stretch-induced Crp3 modulates vein remodeling in response to arterialization by sensitizing SMC to apoptosis.

Smooth muscle cell (SMC) contractility is essential to vessel tone maintenance and blood pressure regulation. In response to vasoconstrictors, calcium-dependent mechanisms promote the activation of the regulatory myosin light chain, leading to increased cytoskeleton tension that favors cell shortening. In contrast, SMC maintain an intrinsic level of a contractile force independent of vasoconstrictor stimulation and sustained SMC contraction beyond the timescale of calcium-dependent mechanisms suggesting the involvement of additional players in the contractile response. Focal adhesions (FAs) are conceivable candidates that may influence SMC contraction. They are required for actin-based traction employed by cells to sense and respond to environmental cues in a process termed mechanotransduction. Depletion of FA proteins impairs SMC contractility, producing arteries that are prone to dissection because of a lack of mechanical stability. Here, we discuss the role of calcium-independent FA signaling mechanisms in SMC contractility. We speculate that FA signaling contributes to the genesis of a variety of SMC phenotypes and discuss the potential implications for mechanical homeostasis in normal and diseased states.

The rate of the remodeling of the arterialized saphenous vein conduit limits the outcomes of coronary artery bypass graft surgery (CABG), which may be influenced by endothelial dysfunction. We tested the hypothesis that high stretch (HS) induces human saphenous vein endothelial cell (hSVEC) dysfunction and examined candidate underlying mechanisms. Our results showed that in vitro HS reduces NO bioavailability, increases inflammatory adhesion molecule expression (E-selectin and VCAM1) and THP-1 cell adhesion. HS decreases F-actin in hSVECs, but not in human arterial endothelial cells, and is accompanied by G-actin and cofilin’s nuclear shuttling and increased reactive oxidative species (ROS). Pre-treatment with the broad-acting antioxidant N-acetylcysteine (NAC) supported this observation and diminished stretch-induced actin remodeling and inflammatory adhesive molecule expression. Altogether, we provide evidence that increased oxidative stress and actin cytoskeleton remodeling play a role in HS-induced saphenous vein endothelial cell dysfunction, which may contribute to predisposing saphenous vein graft to failure.

Vascular aging is accompanied by the fragmentation of elastic fibers and collagen deposition, leading to reduced distensibility and increased vascular stiffness. A rigid artery facilitates elastin to degradation by MMPs, exposing vascular cells to greater mechanical stress and triggering signaling mechanisms that only exacerbate aging, creating a self-sustaining inflammatory environment that also promotes vascular calcification. In this review, we highlight the role of crosstalk between smooth muscle cells and the vascular extracellular matrix (ECM) and how aging promotes smooth muscle cell phenotypes that ultimately lead to mechanical impairment of aging arteries. Understanding the underlying mechanisms and the role of associated changes in ECM during aging may contribute to new approaches to prevent or delay arterial aging and the onset of cardiovascular diseases.

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Agradeço àquele de quem toda sabedoria e conhecimento emanam-Deus que, apesar de Sua infinita grandeza e mesmo eu não sendo merecedor, me lapidou dia após dia desde o meu nascimento de forma que este trabalho fosse desenvolvido. Faltam-me palavras para expressar a minha gratidão. Às pessoas mais nobres que já conhecimeus pais, por incansavelmente suportarem o fardo representado pela criação de alguém como eu, por entenderem os momentos de ausência (que foram muitos) e por fornecerem o suporte necessário para que eu fosse capaz de desenvolver este trabalho. É uma honra ser filho de vocês. Às minhas irmãs, Ester e Nicole, por todo o carinho e compreensão, em especial à Nicole, por ser colírio para os olhos e conforto ao coração sempre, por me entender melhor do que ninguém e sempre buscar fazer o seu melhor para me agradar: palavras falham na tarefa de expressar meu carinho por vocês. Aos meus familiares maternos, especialmente aos meus tios Edilson, Edvaldo, Silvia, Valmir e à minha avó Letícia, por me apoiarem e acreditarem em mim mesmo quando eu estive em dúvida. Este trabalho não existiria se não fosse por vocês, muito obrigado! Ao meu orientador, Prof. Dr. José Eduardo Krieger, por me conceder o privilégio de ser parte do seu time no Laboratório de Genética e Cardiologia Molecular, pelos desafios e pela contribuição à edificação da minha carreira científica. À minha mãe (versão científica), Dra. Ayumi Aurea Miyakawa, por confiar a mim o projeto do qual este trabalho deriva, por acreditar no meu potencial, por me compreender e pela paciência em todos os dias me ensinar a lidar com as nuances que fogem ao nosso controle no meio científico. Ser seu pupilo e parte de sua equipe tem sido enriquecedor desde o princípio. À Renata Carmona, por me receber de braços abertos no Laboratório de Genética e Cardiologia Molecular, pela paciência, pelo apoio nos momentos difíceis e pela receptividade constante às minhas críticas e sugestões. À Dra. Miriam Alaniz, por me compreender nas horas de desespero, por compartilhar sua experiência comigo nos momentos oportunos e pela ajuda incansável na bancada. Ao querido Dr. Mário Costa Cruz da Central de Facilidades para Pesquisa (CEFAP, USP), por todo o tempo dedicado à otimização dos meus ensaios, pelo auxílio na obtenção das imagens, pelos conselhos e por dividir comigo sua vasta experiência científica e de vida. Você simplesmente não existe, Mário!