In a groundbreaking stride toward the future of quantum technology, researchers have unlocked a new mechanism to control quantum emitters embedded in hexagonal boron nitride (hBN), a layered two-dimensional material. This breakthrough could serve as a critical leap forward in integrating quantum emitters into practical devices, bringing quantum computing, secure quantum communications, and ultra-sensitive quantum sensors closer to reality. This promising development emerged from meticulous experimental studies demonstrating the ability to reversibly tune the color and wavelength of light emitted by quantum defects in hBN simply by twisting its atomic layers.

Quantum emitters are nanoscopic sources of light that emit photons with quantum characteristics, pivotal for next-generation technologies reliant on quantum information processing. However, a formidable challenge in utilizing these emitters has been the difficulty in precisely controlling their optical properties post-fabrication. Dr. Angus Gale, the lead scientist behind this research, elucidated how their work provides an innovative “lever” by exploiting the intrinsic layered nature of hBN to adjust the quantum emission properties dynamically. Unlike traditional solid-state hosts such as diamond or silicon carbide, whose structures are rigid and three-dimensional, hBN’s atomically thin layers can be mechanically manipulated, lending itself to an unprecedented degree of tunability.

The team’s experiments demonstrated that by picking up, stacking, twisting, and restacking these ultra-thin hBN slices at varied angles, they could modulate the quantum emitters’ light emission dramatically. These shifts in wavelength were not minor perturbations but substantial changes far exceeding what has been typically achievable in similar solid-state quantum systems. This finding challenges the traditional paradigm which often seeks to stabilize quantum defect behavior within rigid host materials. Instead, the researchers embraced the inherent flexibility and twistability of hBN to realize a new class of quantum control.

Professor Igor Aharonovich, the supervising author, emphasized the broader implications of this twist-controlled modulation approach. He noted that coupling two-dimensional materials at specific twist angles opens up an entirely fresh set of physical phenomena that were previously inaccessible. By assembling layers with precision angular misalignment, new quantum states can emerge, potentially transforming the landscape of material engineering for quantum applications. This strategic layering and twisting, known as “twistronics,” has already inspired revolutionary advances in graphene-based systems, yet this study extends the concept into the realm of quantum emitters embedded in hBN.

One key advantage of using hBN is that its layered crystal structure allows researchers to systematically alter the interaction between layers, effectively tuning the electronic environment surrounding the defects responsible for quantum light emission. As Dr. Gale metaphorically illustrated, far from being a solid block, hBN behaves more like a stack of cheese slices. Just as peeling and recombining slices of cheese can change how flavors intermingle, twisting hBN slices changes the interaction between atomic planes, which in turn alters quantum emitter characteristics. This mechanical engineering at the nanoscale provides a versatile platform for on-demand tuning of quantum light sources.

This technology breakthrough is fundamentally experimental but holds widespread implications. Adjustable quantum emitters could accelerate the development of quantum computing hardware, where precise photon control is essential for encoding and manipulating qubits. Similarly, secure quantum communication protocols rely on tailored quantum light sources to guarantee the generation and distribution of entangled photons immune to interception. Moreover, quantum sensing that exploits the extreme sensitivity of quantum states to environmental changes stands to benefit significantly from tunable quantum emitters, pushing the boundaries of detection limits in fields ranging from medicine to navigation.

Another remarkable facet of the research is the ability to repeatedly pick up, twist, and restack hBN layers without degrading the quantum emitter properties. This reversibility enables iterative fine-tuning of device characteristics and might yield adaptable quantum systems reconfigurable post-production, a feature highly desirable from a technological deployment perspective. This contrasts sharply with permanent structural modifications used in conventional quantum emitter fabrication, which restrict adjustable control and device flexibility.

The team’s methodology involved sophisticated nanofabrication techniques and high-resolution optical spectroscopy to probe the quantum emitters’ response to twist-induced modifications. By correlating the angular misalignment with spectral shifts in emitted light, they constructed a detailed understanding of the underlying physics governing emission control. These insights provide a blueprint for engineering tailored quantum emitters with bespoke characteristics suitable for specific applications.

The research findings have been detailed in a paper published in the eminent journal Science Advances, signaling the scientific community’s enthusiasm for the potential unlocked by twistable quantum systems. Importantly, the authors have declared no competing interests, affirming the independent and foundational nature of this inquiry. Funded by the Australian Research Council and the Air Force Office of Scientific Research, the work highlights the vibrant collaboration between academic institutions and funding bodies committed to propelling quantum technologies.

This discovery heralds a new era in quantum material science, where layered two-dimensional crystals are no longer passive hosts but active tunable platforms. By harnessing the mechanical and electronic versatility of materials like hBN, researchers are gradually unlocking complex quantum phenomena with precision control previously deemed unachievable. The implications extend well beyond fundamental research, marking exciting progress toward quantum devices that could redefine computational power, information security, and sensory precision globally.

In summary, the twist-controlled modulation of quantum emitters in hexagonal boron nitride exemplifies the convergence of cutting-edge experimental physics and materials science innovation. By capitalizing on the unique layered architecture of hBN and the emerging discipline of twistronics, this research pioneers functional tunability in quantum light sources. As the scientific community continues to develop and refine these approaches, we edge closer to the practical implementation of quantum technologies that promise profound societal and technological transformation.

Subject of Research: Not applicable

Article Title: Twist-controlled modulation of quantum emitters in hexagonal boron nitride

News Publication Date: 19-Jun-2026

Web References: 10.1126/sciadv.aec0101

References:

• Gale, A., Aharonovich, I., et al. Twist-controlled modulation of quantum emitters in hexagonal boron nitride. Science Advances. 19 June 2026.

Keywords:
Quantum mechanics, Hexagonal boron nitride, Two-dimensional materials, Quantum emitters, Twistronics, Quantum light sources, Quantum computing, Quantum communication, Quantum sensing, Layered materials, Nanofabrication, Photonic modulation

Atherosclerosis remains the foremost cause of cardiovascular disease-related morbidity and mortality globally, posing a substantial challenge to healthcare systems. Although traditional risk factors such as diet, lifestyle, and genetics have been extensively studied, recent advances have illuminated the pivotal role played by epigenetic mechanisms in shaping the onset and progression of atherosclerotic disease. Epigenetics, the reversible modulation of gene expression without alterations to the DNA sequence, encompasses DNA methylation, histone modifications, and non-coding RNAs, all of which intricately orchestrate cellular behavior within vascular tissues.

Emerging research reveals that DNA methylation patterns, both globally across the genome and in gene-specific loci, critically regulate cellular proliferation and inflammatory responses integral to atherogenesis. Hypomethylation or hypermethylation at particular sites can drastically affect the transcriptional activity of genes responsible for maintaining vascular homeostasis. This phenomenon underscores a dynamic regulatory system where environmental cues and pathological stimuli can induce lasting epigenomic changes that propagate vascular dysfunction and inflammation.

Histone post-translational modifications add another sophisticated layer to this epigenetic landscape. Primarily involving acetylation and methylation of histone proteins, these modifications influence chromatin structure and, consequently, gene accessibility. Within atherosclerotic plaques, histone modifications have been shown to govern networks of genes related to lipid metabolism, cellular plasticity, and inflammatory signaling. Such modifications enable vascular cells to adapt to inflammatory and metabolic stress by modulating transcriptional programs essential for plaque development and instability.

Non-coding RNAs have further expanded the complexity of epigenetic regulation within the vascular milieu. Long non-coding RNAs (lncRNAs) shape the transcriptomic profiles of specific cell types and exert control over the localization and activity of epigenetic enzymes. This targeting ensures that epigenetic remodeling is not only precise but also tailored to cellular needs in the context of vascular remodeling. Concurrently, microRNAs (miRNAs), small regulatory RNAs, predominantly mediate post-transcriptional gene silencing but have been identified to participate in non-canonical functions that influence vascular cell phenotype and immune responses.

The integration of multi-omics approaches, combining epigenomics, transcriptomics, and proteomics, has revolutionized our understanding of the cell-specific epigenetic contributions in atherosclerosis. These technological advancements enable the dissection of complex intercellular interactions within plaques and facilitate the mapping of genetically associated loci to discrete epigenetic modifications. This multidimensional insight is vital to unraveling the heterogeneity of atherosclerotic lesions and their diverse clinical manifestations.

In vascular endothelial cells, epigenetic alterations modulate barrier function, inflammation, and response to shear stress, all of which are critical in the initial stages of atherogenesis. Endothelial dysfunction triggered by epigenetic dysregulation sets the stage for immune cell recruitment and plaque formation. Meanwhile, vascular smooth muscle cells (VSMCs) exhibit remarkable plasticity through epigenetic reprogramming that drives their phenotypic switch from a contractile to a synthetic state, facilitating extracellular matrix remodeling and plaque stability or vulnerability.

Immune cells within the atherosclerotic microenvironment are also subject to profound epigenetic modulation. Macrophages, T cells, and other leukocytes display distinct epigenetic signatures that influence their activation states and inflammatory profiles. Epigenetic memory within these immune populations can perpetuate chronic vascular inflammation, underscoring the need for targeted interventions that modulate immune cell epigenomes to mitigate atherosclerotic progression.

Preclinical studies have leveraged these mechanistic insights to explore epigenetic drug candidates capable of attenuating plaque burden and vascular inflammation. Histone deacetylase inhibitors, DNA methylation modulators, and RNA-based therapeutics have demonstrated efficacy in experimental models, highlighting their potential to recalibrate aberrant gene expression patterns driving disease. However, challenges remain in achieving cell-type specificity, minimizing off-target effects, and ensuring the durability and safety of such interventions in humans.

A critical hurdle for translational success lies in the delivery mechanisms for epigenetic therapies. Nanoparticle-based systems and ligand-targeted delivery platforms are under investigation to enhance precision targeting of vascular and immune cells within plaques. These delivery technologies aim to maximize therapeutic benefit while circumventing systemic toxicity, thereby advancing the clinical applicability of epigenetic modulators.

Long-term safety is another paramount consideration as epigenetic drugs inherently affect gene regulation, potentially leading to unforeseen consequences. Rigorous preclinical evaluation and carefully designed clinical trials are imperative to balance efficacy with safety, ensuring that epigenetic therapies can be integrated into cardiovascular medicine without triggering deleterious off-target effects.

The prospect of leveraging epigenetic regulation heralds a transformative shift in cardiovascular therapeutics, enabling precision medicine tailored to an individual’s unique epigenomic landscape. By elucidating the dynamic and reversible nature of epigenetic modifications in vascular cells and immune populations, researchers are charting new pathways to mitigate atherosclerosis beyond conventional lipid-lowering and anti-inflammatory strategies.

Continued exploration into the interplay between genetic predisposition and environmental influences mediated by epigenetic mechanisms promises to deepen our understanding of atherosclerosis pathobiology. This holistic view integrates molecular, cellular, and systemic insights, empowering the development of sophisticated therapeutics capable of interrupting the disease process at its regulatory roots.

In summary, the frontier of atherosclerosis research lies at the intersection of epigenetics and vascular biology. The potential to manipulate gene expression programs with high specificity and reversibility offers an unprecedented opportunity to combat the global burden of cardiovascular disease. As the field advances, collaboration across disciplines and innovative technological approaches will be essential to realize the therapeutic promise of epigenetic modulation in clinical practice.

With ongoing efforts focused on unraveling cell-specific epigenetic mechanisms, refining drug delivery technologies, and ensuring long-term treatment safety, the era of epigenetics-driven precision cardiology is on the horizon. This paradigm shift not only holds the key to diminishing the impact of atherosclerosis but also exemplifies the broader potential of epigenetic therapies across complex diseases.

Subject of Research: Epigenetic regulation mechanisms in atherosclerosis and their potential for therapeutic intervention.

Article Title: Epigenetic regulation in atherosclerosis and its therapeutic potential

Article References:
Santovito, D., Atzler, D. & Weber, C. Epigenetic regulation in atherosclerosis and its therapeutic potential. Nat Rev Cardiol (2026). https://doi.org/10.1038/s41569-026-01313-8

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