Nickel is a critical element in the shift to sustainable energy systems, with the demand for nickel projected to exceed 6 million tons annually by 20401-4, largely driven by the electrification of the transport sector. Primary nickel production uses acids and carbon-based reductants, emitting about 20 tons of carbon dioxide per ton of nickel produced5-7. Here we present a method using fossil-free hydrogen-plasma-based reduction to extract nickel from low-grade ore variants known as laterites. We bypass the traditional multistep process and combine calcination, smelting, reduction and refining into a single metallurgical step conducted in one furnace. This approach produces high-grade ferronickel alloys at fast reduction kinetics. Thermodynamic control of the atmosphere of the furnace enables selective nickel reduction, yielding an alloy with minimal impurities (<0.04 wt% silicon, approximately 0.01 wt% phosphorus and <0.09 wt% calcium), eliminating the need for further refining. The proposed method has the potential to be up to about 18% more energy efficient while cutting direct carbon dioxide emissions by up to 84% compared with current practice. Our work thus shows a sustainable approach to help resolve the contradiction between the beneficial use of nickel in sustainable energy technologies and the environmental harm caused by its production.

Hydrogen embrittlement (HE) impairs the durability of aluminium (Al) alloys and hinders their use in a hydrogen economy1-3. Intermetallic compound particles in Al alloys can trap hydrogen and mitigate HE4, but these particles usually form in a low number density compared with conventional strengthening nanoprecipitates. Here we report a size-sieved complex precipitation in Sc-added Al-Mg alloys to achieve a high-density dispersion of both fine Al3Sc nanoprecipitates and in situ formed core-shell Al3(Mg, Sc)2/Al3Sc nanophases with high hydrogen-trapping ability. The two-step heat treatment induces heterogeneous nucleation of the Samson-phase Al3(Mg, Sc)2 on the surface of Al3Sc nanoprecipitates that are only above 10 nm in size. The size dependence is associated with Al3Sc nanoprecipitate incoherency, which leads to local segregation of magnesium and triggers the formation of Al3(Mg, Sc)2. The tailored distribution of dual nanoprecipitates in our Al-Mg-Sc alloy provides about a 40% increase in strength and nearly five times improved HE resistance compared with the Sc-free alloy, reaching a record tensile uniform elongation in Al alloys charged with H up to 7 ppmw. We apply this strategy to other Al-Mg-based alloys, such as Al-Mg-Ti-Zr, Al-Mg-Cu-Sc and Al-Mg-Zn-Sc alloys. Our work showcases a possible route to increase hydrogen resistance in high-strength Al alloys and could be readily adapted to large-scale industrial production.

A high-fat, low-fibre Western-style diet (WD) induces microbiome dysbiosis characterized by reduced taxonomic diversity and metabolic breadth1,2, which in turn increases risk for a wide array of metabolic3-5, immune6 and systemic pathologies. Recent work has established that WD can impair microbiome resilience to acute perturbations such as antibiotic treatment7,8, although little is known about the mechanism of impairment and the specific consequences for the host of prolonged post-antibiotic dysbiosis. Here we characterize the trajectory by which the gut microbiome recovers its taxonomic and functional profile after antibiotic treatment in mice on regular chow (RC) or WD, and find that only mice on RC undergo a rapid successional process of recovery. Metabolic modelling indicates that a RC diet promotes the development of syntrophic cross-feeding interactions, whereas in mice on WD, a dominant taxon monopolizes readily available resources without releasing syntrophic byproducts. Intervention experiments reveal that an appropriate dietary resource environment is both necessary and sufficient for rapid and robust microbiome recovery, whereas microbial transplant is neither. Furthermore, prolonged post-antibiotic dysbiosis in mice on WD renders them susceptible to infection by the intestinal pathogen Salmonella enterica serovar Typhimurium. Our data challenge widespread enthusiasm for faecal microbiota transplant (FMT) as a strategy to address dysbiosis, and demonstrate that specific dietary interventions are, at a minimum, an essential prerequisite for effective FMT, and may afford a safer, more natural and less invasive alternative.

The ability to evaluate valence of a social agent based on social experience is essential for an animal's survival in its social group1. Although hippocampal circuits have been implicated in distinguishing novel and familiar conspecifics2-7, it remains unclear how social valence is constructed on the basis of social history and what mechanisms underlie the heightened valence versatility in dynamic relationships. Here we demonstrate that the ventral (v)CA1 integrates serotonin (5-HT) inputs from the dorsal raphe and neurotensin inputs from the paraventricular nucleus of the thalamus (PVT) to determine positive or negative valence of conspecific representations. Specifically, during an appetitive social interaction 5-HT is released into the vCA1 and disinhibits pyramidal neurons through 5-HT1B receptors, whereas neurotensin is released during an aversive social interaction and potentiates vCA1 neurons directly through NTR1s. Optogenetic silencing of dorsal raphe 5-HT and PVT neurotensin inputs into the vCA1 impairs positive and negative social valence, respectively, and excitation flexibly switches valence assignment. These results show how aversive and rewarding social experiences are linked to conspecific identity through converging dorsal raphe 5-HT and PVT neurotensin signals in the vCA1 that instruct opposing valence, and represent a synaptic switch for flexible social valence computation.

In most complex nervous systems there is a clear anatomical separation between the nerve cord, which contains most of the final motor outputs necessary for behaviour, and the brain. In insects, the neck connective is both a physical and an information bottleneck connecting the brain and the ventral nerve cord (an analogue of the spinal cord) and comprises diverse populations of descending neurons (DNs), ascending neurons (ANs) and sensory ascending neurons, which are crucial for sensorimotor signalling and control. Here, by integrating three separate electron microscopy (EM) datasets1-4, we provide a complete connectomic description of the ANs and DNs of the Drosophila female nervous system and compare them with neurons of the male nerve cord. Proofread neuronal reconstructions are matched across hemispheres, datasets and sexes. Crucially, we also match 51% of DN cell types to light-level data5 defining specific driver lines, as well as classifying all ascending populations. We use these results to reveal the anatomical and circuit logic of neck connective neurons. We observe connected chains of DNs and ANs spanning the neck, which may subserve motor sequences. We provide a complete description of sexually dimorphic DN and AN populations, with detailed analyses of selected circuits for reproductive behaviours, including male courtship6 (DNa12; also known as aSP22) and song production7 (AN neurons from hemilineage 08B) and female ovipositor extrusion8 (DNp13). Our work provides EM-level circuit analyses that span the entire central nervous system of an adult animal.

During the twentieth century, inflammatory bowel disease (IBD) was considered a disease of early industrialized regions in North America, Europe and Oceania1. At the turn of the twenty-first century, IBD incidence increased in newly industrialized and emerging regions in Africa, Asia and Latin America, while the prevalence in early industrialized regions continued to grow steadily2-4. Changes in the incidence and prevalence denote the evolution of IBD across four epidemiologic stages: stage 1 (emergence), characterized by low incidence and prevalence; stage 2 (acceleration in incidence), marked by rapidly rising incidence and low prevalence; and stage 3 (compounding prevalence), where the incidence decelerates, plateaus or declines while the prevalence steadily increases. A fourth stage (prevalence equilibrium) has been proposed in which the prevalence slope plateaus due to demographic shifts in an ageing IBD population, but it has not yet been evidenced. To date, these stages have remained theoretical, lacking specific numerical indicators to define transition points. Here, using real-world data from 522 population-based studies encompassing 82 global regions and spanning more than a century (1920-2024), we show spatiotemporal transitions across stages 1-3 and model stage 4 progression. Understanding the evolution of IBD across epidemiologic stages enables healthcare systems to better anticipate the future worldwide burden of IBD.

Neuronal activity must be regulated in a narrow permissive band for the proper operation of neural networks. Changes in synaptic connectivity and network activity-for example, during learning-might disturb this balance, eliciting compensatory mechanisms to maintain network function1-3. In the neocortex, excitatory pyramidal cells and inhibitory interneurons exhibit robust forms of stabilizing plasticity. However, although neuronal plasticity has been thoroughly studied in pyramidal cells4-8, little is known about how interneurons adapt to persistent changes in their activity. Here we describe a critical cellular process through which cortical parvalbumin-expressing (PV+) interneurons adapt to changes in their activity levels. We found that changes in the activity of individual PV+ interneurons drive bidirectional compensatory adjustments of the number and strength of inhibitory synapses received by these cells, specifically from other PV+ interneurons. High-throughput profiling of ribosome-associated mRNA revealed that increasing the activity of a PV+ interneuron leads to upregulation of two genes encoding multiple secreted neuropeptides: Vgf and Scg2. Functional experiments demonstrated that VGF is critically required for the activity-dependent scaling of inhibitory PV+ synapses onto PV+ interneurons. Our findings reveal an instructive role for neuropeptide-encoding genes in regulating synaptic connections among PV+ interneurons in the adult mouse neocortex.

Volcanic hotspots are thought to form by melting in an upwelling mantle plume head followed by melting of the plume tail. Plate motion then generates an age-progressive volcanic track originating from a large igneous province to a currently active hotspot. The most voluminous large igneous province, the approximately 120-million-year-old Ontong Java Nui Plateau (OJP-Nui) in the mid-Pacific, however, lacks an obvious volcanic track. Although the Louisville hotspot track was originally proposed as a candidate, limited constraints for Pacific absolute plate and plume motion before 80 million years ago (Ma) suggest a mismatch1. Existing Pacific models rely on age-distance data from the continuous Hawai'i-Emperor and Louisville tracks, but their tracks older than approximately 80 Ma are subducted. Elsewhere on the Pacific Plate, only discontinuous seamount tracks that formed before 80 Ma are documented2-7. Currently, models require approximately 1,200 kilometres of latitudinal motion to link the Louisville plume to the OJP-Nui1, but palaeolatitude estimates from about 70 Ma to today remain within error of its present location8,9, suggesting that any substantial Louisville plume motion occurred earlier. Here, through a combination of geochemistry and geochronology9-14, we demonstrate that Samoa and Rurutu-Arago are the longest-lived Pacific hotspots, traceable to more than 100 Ma before subducting into the Mariana Trench. These tracks better constrain plate rotation between 80 Ma and 100 Ma, allowing us to update Pacific absolute plate motion models and link the Louisville volcanic track to OJP-Nui without requiring major plume motion.

Nuclear fission leads to the splitting of a nucleus into two fragments1,2. Studying the distribution of the masses and charges of the fragments is essential for establishing the fission mechanisms and refining the theoretical models3,4. It has value for our understanding of r-process nucleosynthesis5,6, in which the fission of nuclei with extreme neutron-to-proton ratios is pivotal for determining astrophysical abundances and understanding the origin of the elements7 and for energy applications8,9. Although the asymmetric distribution of fragments is well understood for actinides (elements in the periodic table with atomic numbers from 89 to 103) based on shell effects10, symmetric fission governs the scission process for lighter elements. However, unexpected asymmetric splits have been observed in neutron-deficient exotic nuclei11, prompting extensive further investigations. Here we present measurements of the charge distributions of fission fragments for 100 exotic fissioning systems, 75 of which have never been measured, and establish a connection between the neutron-deficient sub-lead region and the well-understood actinide region. These new data comprehensively map the asymmetric fission island and provide clear evidence for the role played by the deformed Z = 36 proton shell of the light fragment in the fission of sub-lead nuclei. Our dataset will help constrain the fission models used to estimate the fission properties of nuclei with extreme neutron-to-proton ratios for which experimental data are unavailable.

Indigenous groups often encounter significant challenges when asserting ancestral claims and cultural affiliations based on oral histories, particularly in the USA where such narratives have historically been undervalued. Although ancient DNA offers a tool to complement traditional knowledge and address gaps in oral history, longstanding disregard for Indigenous sovereignty and beliefs has understandably led many Indigenous communities to distrust DNA studies1-4. Earlier research often focused on repatriation claims5-7, whereas more recent work has increasingly moved towards enhancing Tribal histories8,9. Here we present a collaborative study initiated by a federally recognized Native American tribe, the sovereign nation of Picuris Pueblo in the Northern Rio Grande region of New Mexico, USA, to address gaps in traditional knowledge and further their understanding of their population history and ancestry. We generated genomes from 16 ancient Picuris individuals and 13 present-day members of Picuris Pueblo, providing genomic data spanning the last millennium. We show genetic continuity between ancient and present-day Picuris, and more broadly with Ancestral Puebloans from Pueblo Bonito in Chaco Canyon10, 275 km to the west. This suggests a firm spatiotemporal link among these Puebloan populations of the North American Southwest. Furthermore, we see no evidence of population decline before European arrival11-13, and no Athabascan ancestry in individuals predating 1500 CE, challenging earlier migration hypotheses14-16. This work prioritizes Indigenous control of genetic data and brings together oral tradition, archaeology, ethnography and genetics.

Matrix-derived biophysical cues are known to regulate the activation of fibroblasts and their subsequent transdifferentiation into myofibroblasts1-6, but whether modulation of these signals can suppress fibrosis in intact tissues remains unclear, particularly in the cardiovascular system7-10. Here we demonstrate across multiple scales that inhibition of matrix mechanosensing in persistently activated cardiac fibroblasts potentiates-in concert with soluble regulators of the TGFβ pathway-a robust transcriptomic, morphological and metabolic shift towards quiescence. By conducting a meta-analysis of public human and mouse single-cell sequencing datasets, we identify the focal-adhesion-associated tyrosine kinase SRC as a fibroblast-enriched mechanosensor that can be targeted selectively in stromal cells to mimic the effects of matrix softening in vivo. Pharmacological inhibition of SRC by saracatinib, coupled with TGFβ suppression, induces synergistic repression of key profibrotic gene programs in fibroblasts, characterized by a marked inhibition of the MRTF-SRF pathway, which is not seen after treatment with either drug alone. Importantly, the dual treatment alleviates contractile dysfunction in fibrotic engineered heart tissues and in a mouse model of heart failure. Our findings point to joint inhibition of SRC-mediated stromal mechanosensing and TGFβ signalling as a potential mechanotherapeutic strategy for treating cardiovascular fibrosis.

Marine plastic pollution is a global issue, with microplastics (1 µm-5 mm) dominating the measured plastic count1,2. Although microplastics can be found throughout the oceanic water column3,4, most studies collect microplastics from surface waters (less than about 50-cm depth) using net tows5. Consequently, our understanding of the microplastics distribution across ocean depths is more limited. Here we synthesize depth-profile data from 1,885 stations collected between 2014 and 2024 to provide insights into the distribution and potential transport mechanisms of subsurface (below about 50-cm depth, which is not usually sampled by traditional practices3,6) microplastics throughout the oceanic water column. We find that the abundances of microplastics range from 10-4 to 104 particles per cubic metre. Microplastic size affects their distribution; the abundance of small microplastics (1 µm to 100 µm) decreases gradually with depth, indicating a more even distribution and longer lifespan in the water column compared with larger microplastics (100 µm to 5,000 µm) that tend to concentrate at the stratified layers. Mid-gyre accumulation zones extend into the subsurface ocean but are concentrated in the top 100 m and predominantly consist of larger microplastics. Our analysis suggests that microplastics constitute a measurable fraction of the total particulate organic carbon, increasing from 0.1% at 30 m to 5% at 2,000 m. Although our study establishes a global benchmark, our findings underscore that the lack of standardization creates substantial uncertainties, making it challenging to advance our comprehension of the distribution of microplastics and its impact on the oceanic environment.

The discovery of ferrocene1 heralded the advent of modern organometallic chemistry. Characterized by the π-coordination of a metal by one or two planar annulene anions, ferrocenes and their analogues2-4 exemplify the archetype of out-of-plane annulene metal complexes. By contrast, the integration of metal within the annulene core to form in-plane annulene metal complexes featuring metal-carbon σ bonds has been obstructed not only by the synthetic difficulty and the non-planarity of annulenes with appropriate internal dimensions, but also by the difficulty of embedding the metal. These challenges have prevented the isolation of such in-plane annulene metal complexes. Here we report the preparation of three metal-centred planar [15]annulene frameworks. The most symmetrical fragment has D5h symmetry, with the metal centre shared by five identical five-membered rings. Density functional theory calculations demonstrate that metal d orbitals participate in conjugation with these five-membered rings, rendering all of them aromatic. The overall framework bears a loose structural and spectroscopic analogy to metallo-expanded porphyrins with multiple aza donors5, which thus provides a nexus between annulene chemistry and classic heteroatom-based coordination chemistry. The present systems display high stability and are easily functionalized. We thus suggest that metal-centred planar annulenes could emerge as promising building blocks for materials science.

Animal and bacterial cells use nucleotidyltransferase (NTase) enzymes to respond to viral infection and control major forms of immune signaling including cGAS-STING innate immunity and CBASS anti-phage defence1-4. Here we discover a family of bacterial defence systems, which we name Hailong, that use NTase enzymes to constitutively synthesize DNA signals and guard against phage infection. Hailong protein B (HalB) is an NTase that converts deoxy-ATP into single-stranded DNA oligomers. A series of X-ray crystal structures define a stepwise mechanism of HalB DNA synthesis initiated by a C-terminal tyrosine residue that enables de novo enzymatic priming. We show that HalB DNA signals bind to and repress activation of a partnering Hailong protein A (HalA) effector complex. A 2.0 Å cryo-EM structure of the HalA-DNA complex reveals a membrane protein with a conserved ion channel domain and a unique crown domain that binds the DNA signal and gates activation. Analyzing Hailong defence in vivo, we demonstrate that viral DNA exonucleases required for phage replication trigger release of the primed HalA complex and induce protective host cell growth arrest. Our results explain how inhibitory nucleotide immune signals can serve as molecular guards against phage infection and expand the mechanisms NTase enzymes use to control antiviral immunity.

Despite accumulating evidence that bat-derived coronaviruses often require intermediate hosts to facilitate transmission to humans1, the potential role of fur animals in zoonotic coronavirus spillovers has largely been overlooked2. Here we report the isolation and characterization of a novel mink respiratory coronavirus (MRCoV) from farmed minks with pneumonia. Notably, MRCoV uses angiotensin-converting enzyme 2 (ACE2) as a receptor and can infect mink, bat, monkey, and human cells. Cryo-electron microscopy analysis revealed that the MRCoV receptor-binding domain (RBD) binds to the same interface on ACE2 receptors as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) RBD, despite exhibiting notable structural differences. We identify the key determinants on ACE2 and MRCoV RBD that confer efficient binding. HKU5-33S, a bat coronavirus closely related to MRCoV, utilizes ACE2 of bat Pipistrellus abramus and requires only two amino acid substitutions to adapt to mink ACE2. Furthermore, SARS-CoV-2 protease and polymerase inhibitors potently block MRCoV infection, indicating a potential therapeutic strategy. Collectively, these findings enhance the understanding of coronavirus receptor dynamics and highlight their zoonotic potential. Given the risks posed by fur farms as reservoirs for emerging pathogens, our study underscores the urgent need for enhanced surveillance to mitigate future coronavirus outbreaks.

Recent advances in quantum communications have underscored the crucial role of optical coherence in developing quantum networks. This resource, which is fundamental to the phase-based architecture of the quantum internet1, has enabled the only successful demonstrations of multi-node quantum networks2-4 and substantially extended the range of quantum key distribution (QKD)5. However, the scalability of coherence-based quantum protocols remains uncertain owing to the specialized hardware required, such as ultra-stable optical cavities and cryogenic photon detectors. Here we implement the coherence-based twin-field QKD protocol over a 254-kilometre commercial telecom network spanning between Frankfurt and Kehl, Germany, achieving encryption key distribution at 110 bits per second. Our results are enabled by a scalable approach to optical coherence distribution, supported by a practical system architecture and non-cryogenic single-photon detection aided by off-band phase stabilization. Our results demonstrate repeater-like quantum communication in an operational network setting, doubling the distance for practical real-world QKD implementations without cryogenic cooling. In addition, to our knowledge, we realized one of the largest QKD networks featuring measurement-device-independent properties6. Our research aligns the requirements of coherence-based quantum communication with the capabilities of existing telecommunication infrastructure, which is likely to be useful to the future of high-performance quantum networks, including the implementation of advanced quantum communication protocols, quantum repeaters, quantum sensing networks and distributed quantum computing7.

Metamaterials with multimodal deformation mechanisms resemble machines1,2, especially when endowed with autonomous functionality. A representative architected assembly, with tunable chirality, converts linear motion into rotation3. These chiral metamaterials with a machine-like dual modality have potential use in areas such as wave manipulation4, optical activity related to circular polarization5 and chiral active fluids6. However, the dual motions are essentially coupled and cannot be independently controlled. Moreover, they are restricted to small deformation, that is, strain ≤2%, which limits their applications. Here we establish modular chiral metamaterials, consisting of auxetic planar tessellations and origami-inspired columnar arrays, with decoupled actuation. Under single-degree-of-freedom actuation, the assembly twists between 0° and 90°, contracts in-plane up to 25% and shrinks out-of-plane more than 50%. Using experiments and simulations, we show that the deformation of the assembly involves in-plane twist and contraction dominated by the rotating-square tessellations and out-of-plane shrinkage dominated by the tubular Kresling origami arrays. Moreover, we demonstrate two distinct actuation conditions: twist with free translation and linear displacement with free rotation. Our metamaterial is built on a highly modular assembly, which enables reprogrammable instability, local chirality control, tunable loading capacity and scalability. Our concept provides routes towards multimodal, multistable and reprogrammable machines, with applications in robotic transformers, thermoregulation, mechanical memories in hysteresis loops, non-commutative state transition and plug-and-play functional assemblies for energy absorption and information encryption.

Will it ever be possible to sue anyone for damaging the climate? Twenty years after this question was first posed, we argue that the scientific case for climate liability is closed. Here we detail the scientific and legal implications of an 'end-to-end' attribution that links fossil fuel producers to specific damages from warming. Using scope 1 and 3 emissions data from major fossil fuel companies, peer-reviewed attribution methods and advances in empirical climate economics, we illustrate the trillions in economic losses attributable to the extreme heat caused by emissions from individual companies. Emissions linked to Chevron, the highest-emitting investor-owned company in our data, for example, very likely caused between US $791 billion and $3.6 trillion in heat-related losses over the period 1991-2020, disproportionately harming the tropical regions least culpable for warming. More broadly, we outline a transparent, reproducible and flexible framework that formalizes how end-to-end attribution could inform litigation by assessing whose emissions are responsible and for which harms. Drawing quantitative linkages between individual emitters and particularized harms is now feasible, making science no longer an obstacle to the justiciability of climate liability claims.

The maritime Phoenician civilization from the Levant transformed the entire Mediterranean during the first millennium BCE1-3. However, the extent of human movement between the Levantine Phoenician homeland and Phoenician-Punic settlements in the central and western Mediterranean has been unclear in the absence of comprehensive ancient DNA studies. Here, we generated genome-wide data for 210 individuals, including 196 from 14 sites traditionally identified as Phoenician and Punic in the Levant, North Africa, Iberia, Sicily, Sardinia and Ibiza, and an early Iron Age individual from Algeria. Levantine Phoenicians made little genetic contribution to Punic settlements in the central and western Mediterranean between the sixth and second centuries BCE, despite abundant archaeological evidence of cultural, historical, linguistic and religious links4. Instead, these inheritors of Levantine Phoenician culture derived most of their ancestry from a genetic profile similar to that of Sicily and the Aegean. Much of the remaining ancestry originated from North Africa, reflecting the growing influence of Carthage5. However, this was a minority contributor of ancestry in all of the sampled sites, including in Carthage itself. Different Punic sites across the central and western Mediterranean show similar patterns of high genetic diversity. We also detect genetic relationships across the Mediterranean, reflecting shared demographic processes that shaped the Punic world.

Acute myocardial infarction is a leading cause of morbidity and mortality worldwide1. Clinical studies have shown that the severity of cardiac injury after myocardial infarction exhibits a circadian pattern, with larger infarcts and poorer outcomes in patients experiencing morning-onset events2-7. However, the molecular mechanisms underlying these diurnal variations remain unclear. Here we show that the core circadian transcription factor BMAL17-11 regulates circadian-dependent myocardial injury by forming a transcriptionally active heterodimer with a non-canonical partner-hypoxia-inducible factor 2 alpha (HIF2A)12-16-in a diurnal manner. To substantiate this finding, we determined the cryo-EM structure of the BMAL1-HIF2A-DNA complex, revealing structural rearrangements within BMAL1 that enable cross-talk between circadian rhythms and hypoxia signalling. BMAL1 modulates the circadian hypoxic response by enhancing the transcriptional activity of HIF2A and stabilizing the HIF2A protein. We further identified amphiregulin (AREG)16,17 as a rhythmic target of the BMAL1-HIF2A complex, critical for regulating daytime variations of myocardial injury. Pharmacologically targeting the BMAL1-HIF2A-AREG pathway provides cardioprotection, with maximum efficacy when aligned with the pathway's circadian phase. These findings identify a mechanism governing circadian variations of myocardial injury and highlight the therapeutic potential of clock-based pharmacological interventions for treating ischaemic heart disease.