Beneath every step we take, soils hold one of the planet’s largest reservoirs of carbon, a vast, slow-moving bank of organic matter that quietly regulates how much of the world’s carbon stays locked away and how much escapes into the atmosphere as greenhouse gas. Now a sweeping new review warns that climate-driven extremes, droughts, floods, and wildfires, are rewriting the rules of that subterranean economy in ways that conventional models and land-management practices have not yet caught up with. The analysis, led by environmental scientist Nanthi Bolan of the University of Western Australia and colleagues, including a corresponding authorship by Bolan himself, synthesizes a substantial body of global evidence on how extreme weather reshapes carbon inputs to soil, microbial processing, erosion, and the sequestration of carbon that underpins soil health, water retention, nutrient cycling, and agricultural productivity.

The work, published in the journal Carbon Research, is notable for the scale of its underlying evidence base. On 14 January 2026, the authors searched Google Scholar, PubMed, and Web of Science using terms spanning climate change, extreme weather, soil carbon, microbial activity, decomposition, erosion, dissolved organic matter, and leaching. The initial sweep returned 14,218 records; after removing duplicates and screening for eligibility, 3,754 articles remained for bibliometric and qualitative analysis. From those, 187 publications were selected for detailed synthesis based on relevance, methodological rigor, and the substantive quality of their findings. Keyword co-occurrence patterns were mapped with VOSviewer, a bibliometric tool that reveals the intellectual architecture of a research field. The result is a critical review grounded in structured literature screening rather than new experimental data, but its synthesis offers one of the most comprehensive maps yet of how extremes rearrange the soil carbon cycle.

The review’s central finding is that no two extremes act alike. Drought, the most widespread disturbance, operates largely through the plant side of the equation. When rainfall fails, photosynthesis slows, plant biomass production falls, and the total flux of carbon entering soils through roots, residues, and litter declines. There is a nuance here: under moderate water stress, plants may temporarily shift a greater proportion of their fixed carbon belowground, investing in roots to chase moisture. But prolonged drought overwhelms that compensatory response. Microbial biomass shrinks, litter decomposition stalls, and the living engine of the soil carbon cycle idles. Then comes the deceptive twist: when rain finally returns, rewetting triggers a rapid pulse of carbon dioxide as starved soil microbes seize upon the accumulated substrates left behind by months of suspended activity. That post-drought CO₂ flush, the review emphasizes, can erase much of the apparent “savings” that accumulated during the dry period. Across the assembled evidence, repeated and multi-year drought was consistently associated with declining soil organic carbon, with grasslands and arable croplands showing particularly pronounced losses, ecosystems that happen to anchor much of the world’s food production.

Flooding tells the opposite story, but it ends in many of the same places. Water saturation chokes off oxygen diffusion through soil pores, forcing microbial metabolism into anaerobic pathways. That shift changes everything downstream. Prolonged waterlogging can drive the chemical reduction of iron oxyhydroxides, minerals that in oxygenated conditions act as microscopic glues binding organic carbon to soil particles. When those minerals dissolve, the carbon they held is released as dissolved organic carbon, which can then be stripped away by erosion and leaching and exported to rivers, lakes, and ultimately the ocean. The review stresses, however, that flooding is not unambiguously a carbon loss story. Wetlands and other periodically inundated ecosystems can accumulate and retain enormous carbon stocks precisely because water constrains decomposition. Whether a flood event releases carbon or banks it depends on the interplay between plant inputs, oxygen availability, and hydrological transport, a delicate balance that shifting rainfall regimes are actively destabilizing.

Wildfire is the most dramatic and immediately visible of the three forces, and its effects cascade on multiple timescales. Combustion directly strips vegetation, litter, and soil organic matter, transferring carbon to the atmosphere in hours. But fire also rearranges the physical and biological landscape of the soil in subtler ways: it can increase erosion by removing protective ground cover, alter soil wettability in ways that change hydrological behavior, restructure microbial communities, and expose previously protected carbon, once shielded inside aggregates or mineral associations, to fresh decomposition. There is a paradoxical bright spot. Pyrogenic carbon, the charcoal-like residue of incomplete combustion, is chemically recalcitrant and can persist in soils for centuries or millennia, functioning as a long-term carbon sink. Whether a fire leaves a landscape as a net carbon source or stabilizes some of its carbon in pyrogenic form depends on fire severity, soil moisture, fuel load, ecosystem type, and the trajectory of post-fire recovery. The review is clear that this balance cannot be predicted from fire alone; it is contingent, site by site, on conditions that vary widely across the globe.

Perhaps the most consequential theme running through the synthesis is that carbon responses cannot be inferred from the type of extreme event alone. Land use, soil mineralogy, hydrology, salinity, vegetation composition, microbial community makeup, and the timing of events within a season all determine whether carbon ends up stored, mobilized, or released. Iron and aluminum oxyhydroxides and clay minerals, for instance, provide mineral protection that can shield organic matter even under stress, while sandy or low-clay soils offer little such refuge. Managed croplands respond differently from native grasslands; saline coastal soils behave differently from acidic forest soils. And compound events, drought followed by wildfire, or alternating drought and flooding in rapid succession, may produce effects that are qualitatively different from those of isolated disturbances, as when a dried landscape burns more intensely, or when post-fire soils, stripped of vegetation, wash away in the first heavy rain. The review argues that the climate science and soil science communities have largely studied these disturbances one at a time, while the real world increasingly delivers them in combination.

The implications for climate mitigation and adaptation are substantial. Soil organic carbon is frequently invoked in national climate pledges and voluntary carbon markets as a bankable sink, yet the review suggests that the security of that bank depends heavily on how often and how severely extremes strike. If multi-year droughts steadily drain carbon from grasslands and croplands, or if fires repeatedly reset accumulation cycles, the effective permanence of soil carbon storage becomes far more fragile than many accounting frameworks assume. Conversely, protecting and rebuilding soil carbon delivers benefits well beyond climate: it improves water retention in drought-prone regions, supports nutrient cycling, stabilizes soil structure against erosion, and sustains the microbial diversity on which fertility depends. Carbon stewardship, in other words, is not separable from food security or ecosystem resilience; it is the same problem viewed from different angles.

The authors are candid about the limits of the current evidence base. The article does not report newly generated datasets and does not present a dedicated limitations section, and its conclusions rest on a qualitative synthesis of selected publications. Consequently, they call for improved and more consistent evidence across soil types, land uses, and both terrestrial and aquatic environments, and across multiple temporal scales, from the instantaneous CO₂ pulse after rewetting to the multi-decadal trajectory of carbon storage. Standardizing measurements of carbon pools, microbial functions, and event intensity, they argue, would make results comparable across ecosystems and enable more confident generalization, something the field currently struggles to achieve given heterogeneous methods and site-specific reporting.

Looking forward, the review sketches a research agenda that is as technologically ambitious as it is mechanistically focused. The authors recommend integrating high-resolution remote sensing with ground observations, advanced spectroscopy, molecular analyses, and integrated modeling to track carbon as it moves through soils and into waterways. They single out several priorities: characterizing microbial genomic and functional diversity as it responds to stress, quantifying carbon stoichiometry, probing the interactions between organic matter and iron and aluminum oxyhydroxides, understanding clay-mineral protection mechanisms, tracking long-term storage outcomes, and systematically studying the sequencing of compound extreme events. Each of these threads addresses a gap in the mechanistic chain that links a weather event in the atmosphere to a molecule of carbon, stabilized or released, in the soil.

What emerges from the review is a picture of the soil carbon cycle not as a stable background process but as a dynamic, contested system whose behavior under climate extremes is far less predictable than once assumed. The same storm that floods a rice paddy and exports carbon to a river delta may, a few hundred kilometers away, end a drought and briefly green a grassland, with opposite consequences for the atmosphere. As extremes grow more frequent and more compound, the review makes the case that understanding, and safeguarding, the carbon held beneath our feet will require science that is as interconnected and as restless as the weather itself.

Keywords

soil organic carbon, extreme weather, drought, flooding, wildfire, carbon sequestration, microbial activity, dissolved organic carbon, erosion, pyrogenic carbon, climate change, soil health

Idiopathic pulmonary fibrosis, a relentlessly progressive and fatal scarring disease of the lungs, has long frustrated clinicians with only two approved drugs that slow but cannot reverse its course. Now, a team of researchers in Taiwan has identified a surprising new player in the disease’s destructive machinery: doublecortin-like kinase 1, or DCLK1, a kinase better known for its role in cancer stem cells. Their study, published in the Journal of Biomedical Science, demonstrates that DCLK1 drives fibroblast activation in the lung and that blocking it—either genetically or with an oral inhibitor—slows fibrosis and preserves lung function in mice. The findings position DCLK1 as a promising therapeutic target in one of medicine’s most stubborn diseases.

The research, led by Lee-Yuan Lin, Wun-Hao Cheng, Chien-Huang Lin and Bing-Chang Chen of Taipei Medical University, together with collaborators at National Taiwan University Hospital and Universitas Gadjah Mada, began with a question that has lingered in the literature. Gene expression analyses had previously hinted that DCLK1 might be implicated in IPF, and earlier work reported that the kinase is markedly enhanced in the alveolar epithelial cells of patients with pulmonary fibrosis and in mice with bleomycin-induced fibrosis. But its function in fibroblast activation—the cellular engine of fibrosis—had remained unexplained.

To begin untangling that role, the team mined a publicly available single-cell RNA sequencing data set containing more than 312,000 cells from healthy lungs, IPF lungs, and lungs with chronic obstructive pulmonary disease. After stringent quality control filtering, they focused on roughly 240,000 cells from the control and IPF groups and mapped DCLK1 expression across the major lung cell lineages: epithelial, endothelial, lymphoid, myeloid, and stromal cells. The signal was unmistakable. DCLK1 was expressed across many cell populations, but the highest expression appeared in the stromal compartment, particularly in myofibroblasts—the specialized, contractile fibroblasts that churn out the extracellular matrix and stiffen lung tissue in IPF.

Human tissue told the same story. The researchers examined lung samples from eleven patients with IPF, obtained during lung transplantation or surgery, alongside fourteen nonfibrotic control samples. Histological staining with hematoxylin and eosin and Masson trichrome confirmed the expected picture of interstitial consolidation and collagen deposition in the IPF specimens. More importantly, immunohistochemistry revealed that both total DCLK1 and its phosphorylated, activated form were significantly upregulated in the fibrotic lung interstitium compared with control tissue. DCLK1, in other words, was not merely present in scarred lungs—it was switched on.

DCLK1 is an intriguing molecule to find at the center of a fibrotic process. It is a serine/threonine kinase belonging to the calcium/calmodulin-dependent kinase family, distinguished by two microtubule-binding domains. In oncology, DCLK1 overexpression has been documented in colorectal, pancreatic, gastric, renal, and hepatocellular carcinomas, where it correlates with poor prognosis, high recurrence, and metastasis, promoting tumor initiation and the epithelial–mesenchymal transition in cancer stem cells. It has also been linked to inflammatory signaling in SARS-CoV-2 infection, where inhibiting it blocks proinflammatory caspase-1/interleukin-1β signaling. The new study extends this portfolio of mischief to the fibrotic lung.

To test causality rather than mere correlation, the researchers turned to mice. They crossed animals carrying loxP sites flanking exon 3 of the DCLK1 locus with Pgk1-RFP-Cre/ERT2 transgenic mice, generating a system in which tamoxifen administration triggers global deletion of the Dclk1 gene. When these DCLK1 knockout mice and littermate controls were given intratracheal bleomycin, a chemotherapy drug used to induce pulmonary fibrosis in laboratory animals, the difference was striking. Knockout mice showed far less lung infiltration and collagen deposition, reduced numbers of cells staining positive for DCLK1 together with fibroblast surface protein and alpha-smooth muscle actin, and significantly lower levels of the profibrotic proteins fibronectin, α-SMA, and connective tissue growth factor, or CTGF.

The protective effect extended well beyond molecular markers. Using the FlexiVent FX system to measure lung mechanics, the team found that bleomycin treatment significantly reduced respiratory system compliance and pressure–volume performance and increased the normalized work of breathing in control mice—hallmarks of a stiffening, fibrotic lung. In the DCLK1 knockout animals, these functional deficits were substantially attenuated. In vivo microcomputed tomography, acquired at 34.75-micrometer voxel resolution, painted the morphological counterpart: bleomycin caused parenchymal destruction and volume loss in control lungs, while knockout mice retained lung structure and volume. Density histograms shifted toward fibrotic tissue in wild-type animals but stayed largely preserved in the knockouts, and peripheral blood neutrophil percentages, which climbed after bleomycin injury, were significantly reduced in the knockout group.

With the in vivo evidence established, the investigators dissected the molecular wiring in cultured normal human lung fibroblasts. Transforming growth factor beta, the master profibrotic cytokine, induced DCLK1 phosphorylation within 30 minutes and DCLK1 expression within 8 hours. Chromatin immunoprecipitation assays showed that after TGF-β stimulation, both Smad3—the canonical transcriptional mediator of TGF-β signaling—and the nuclear factor kappa B subunit p65 enriched at the DCLK1 promoter, indicating that TGF-β switches on DCLK1 through both Smad-dependent and noncanonical NF-κB pathways. Silencing DCLK1 with small interfering RNA then blunted the fibroblast’s profibrotic response, reducing TGF-β-induced expression of fibronectin, collagen 1A1, α-SMA, and CTGF.

The pathway, however, does not stop there. The team found that TGF-β also phosphorylated Akt, and that transfecting fibroblasts with a dominant-negative Akt construct reduced TGF-β-induced DCLK1 phosphorylation and the expression of fibronectin and CTGF—placing Akt upstream of DCLK1. Downstream, DCLK1 knockdown reduced Smad3 phosphorylation while DCLK1 overexpression enhanced it. Coimmunoprecipitation revealed a physical association between DCLK1 and Smad3, and immunofluorescence microscopy showed the two proteins colocalizing in the nucleus within 30 minutes of TGF-β treatment. A ChIP assay using a DCLK1 antibody pulled down DNA from the Smad3-binding region of the CTGF promoter, and pretreatment with the selective DCLK1 inhibitor DCLK1-IN-1 reduced TGF-β-induced CTGF expression. Together, the results sketch an Akt/DCLK1/Smad3 axis through which TGF-β drives the production of connective tissue growth factor, a potent profibrotic mediator.

The clinical payoff came in the pharmacological arm of the study. Mice receiving oral DCLK1-IN-1 at 10 milligrams per kilogram daily, beginning on day 7 after bleomycin instillation and continuing until day 28, showed visibly reduced fibrotic progression on histology, lower expression of fibronectin, α-SMA, and CTGF in lung tissue and lysates, preserved pulmonary compliance, improved pressure–volume loops, and reduced work of breathing. Serial microCT scans on days 7, 17, and 27 documented less severe fibrotic remodeling in the treated animals, with lung attenuation histograms showing a smaller fraction of dense, nonaerated voxels. Blood neutrophil counts were also lower. In short, a pill-like oral inhibitor measurably slowed the disease in a model that mirrors the human condition.

The implications are significant because the current therapeutic landscape for IPF is so thin. Only nintedanib, a tyrosine kinase inhibitor targeting growth factor receptors, and pirfenidone, which suppresses TGF-β production and activity, are approved by the US Food and Drug Administration, and both merely slow progression. The recent failure of pamrevlumab, a monoclonal antibody against CTGF, in the phase 3 ZEPHYRUS-1 trial suggested that targeting downstream fibrotic end products alone may be insufficient—pointing to the value of upstream signaling regulators such as DCLK1. Adding to the appeal, a DCLK1 inhibitor has already been shown to prevent inflammatory responses in acute lung injury, hinting at dual anti-fibrotic and anti-inflammatory potential.

The authors are careful to note limitations. DCLK1 is expressed across multiple lung cell types, and the tamoxifen-inducible knockout used here was global rather than cell-type-specific, so the contributions of fibroblasts versus epithelial, endothelial, and immune cells could not be fully separated. Human control tissue, as in most fibrosis studies, came from heterogeneous sources, including tumor-adjacent lung. The precise subcellular mechanics of the DCLK1–Smad3 interaction, whether DCLK1 inhibition can promote fibrosis resolution rather than merely slow progression, and the systemic safety of long-term DCLK1 blockade—all relevant given the kinase’s role in cancer and other processes—remain open questions.

Even so, the convergence of evidence is striking: DCLK1 is upregulated in human IPF, amplified in experimental fibrosis, mechanistically coupled to the TGF-β–Smad3 engine of fibroblast activation, and its suppression by both genetics and a small molecule preserves lung structure and function. What began as a cancer stem cell marker has now emerged, unexpectedly, as a central node in the scarring of the lung—offering fresh hope that a disease long considered irreversible may one day be stopped at its molecular source.

In a finding that could reshape how ophthalmologists think about one of the most delicate complications of corneal surgery, a team of computational engineers has built the first detailed computer model of a human eye in which the Descemet membrane—the paper-thin basement layer at the back of the cornea—has become detached. By simulating the fluid–structure interaction between the aqueous humor sloshing inside the eye’s anterior chamber and the flexible, detached membrane itself, the researchers have produced quantitative predictions about the mechanical stresses such a detachment imposes, and about how different transplanted corneas might alter those stresses during post-operative thermal therapy.

The study, published in the Annals of Biomedical Engineering, addresses a long-standing blind spot in ocular biomechanics. Detachment of the Descemet membrane is a recognized complication of cataract surgery, corneal transplantation and certain corneal dystrophies, and it can cause significant corneal swelling and vision loss if the membrane does not reattach. Yet most previous computational examinations of the anterior chamber have treated the eye’s interior as rigid-walled plumbing, focusing on fluid flow or heat transfer while excluding the complex two-way coupling between the intraocular fluid and the fragile ocular structures suspended within it. The new work changes that by modeling the detached Descemet membrane as a deformable, elastic solid that bends, stretches and deforms under the pressure and shear of the aqueous humor flowing around it.

The researchers, led by Ammar I. Alsabery of the Islamic University in Najaf, Iraq, together with colleagues from the University of Basrah, King Khalid University in Saudi Arabia, Saveetha School of Engineering in India, and Universiti Kebangsaan Malaysia, employed a coupled numerical scheme that solves simultaneously for the buoyancy-driven flow of aqueous humor and for the structural deformation of the membrane. The geometry represents the anterior chamber—the fluid-filled space between the cornea and the iris—with a warm region corresponding to the lens contact zone held at an isothermal hot temperature, mimicking the thermal gradients that arise in ocular warming therapies and in normal physiological conditions.

At the heart of the analysis is the Rayleigh number, a dimensionless parameter that governs the strength of natural convection: warmer, less dense fluid rises while cooler fluid sinks, generating circulating currents within the chamber. The team varied the Rayleigh number across three orders of magnitude, from 10³ to 10⁶, which corresponds to temperature differences spanning from a fraction of a degree to 250 Kelvin. This range deliberately encompasses both the mild thermal gradients present in the living eye and the much more aggressive temperature differences applied during clinical thermal therapy of the cornea, allowing the same model to speak to both resting physiology and active treatment.

Equally central to the study is the elasticity modulus of the detached membrane. The researchers swept this property across nine orders of magnitude, from 10⁸ to 10¹¹, a range designed to represent everything from highly compliant, freshly detached tissue to the much stiffer mechanical character of donor corneal tissue used in transplantation. Because the Descemet membrane’s stiffness varies with age, disease state and surgical history, this parametric approach lets the model answer a question that clinicians genuinely care about: does the type of cornea grafted into a patient change the mechanical load experienced by a detached membrane during recovery? The answer, according to the simulations, is nuanced. The cornea type does affect the stress imparted on the detached Descemet membrane, but it does not affect the thermal characteristics of the anterior chamber or the overall displacement behavior within it. In other words, stiffer transplanted tissue changes the mechanical environment at the membrane itself without appreciably altering the convective heat transfer patterns of the aqueous humor circulating beneath it.

The fluid dynamics of the anterior chamber turned out to be far more sensitive to geometry than to tissue stiffness. One of the most striking results concerns the iris, the pigmented diaphragm whose length in the model determines the extent of the hot, isothermal contact region associated with the lens. When the team simulated a shrinkage of the iris—effectively reducing the length of the contacting part of the lens held at the hot temperature—they found that the convective thermal characteristic of the anterior chamber rose by approximately 78 percent. This dramatic enhancement arises because the reduced iris length reshapes the buoyancy-driven circulation cells, allowing warmer fluid to travel more freely and exchange heat more efficiently with its surroundings. For clinicians, the implication is that the geometry of the anterior chamber, shaped in part by the iris and the lens, is a first-order determinant of how heat is distributed during thermal therapy, potentially more important than the material properties of the graft itself.

The temperature difference applied during thermal therapy also proved to be a powerful lever. Raising the applied thermal gradient from 2.5 Kelvin to 25 Kelvin—a tenfold increase—promoted heat transfer within the anterior chamber by 47.6 percent. While the scaling is sublinear rather than directly proportional to the temperature difference, the result confirms that modest increases in therapeutic temperature can yield meaningful gains in convective heat delivery without requiring a hundredfold jump in applied thermal load. The finding offers a quantitative framework for calibrating thermal treatments of the anterior segment: therapy protocols could, in principle, be tuned to achieve target heat transfer rates while respecting the narrow thermal safety margins of living ocular tissue.

Technically, the simulations belong to a class of problems known as fluid–structure interaction, or FSI, in which the fluid equations and the solid mechanics equations are coupled and solved together rather than in isolation. In this case, the aqueous humor—an essentially water-like fluid—drives natural convection under the influence of gravity, while the detached Descemet membrane responds to the pressure and viscous stresses exerted by that flow. The membrane’s deformation, in turn, modifies the shape of the fluid domain, feeding back into the flow field. This two-way coupling is computationally demanding but essential, because a rigid-wall approximation would entirely miss the bending and displacement of the detached membrane, along with the localized stress concentrations that could determine whether the membrane reattaches, tears further, or remains stable during healing. The methodology builds on the team’s earlier FSI studies of flexible fins, baffles and partitions in convective systems, as well as their prior work applying FSI modeling to blood flow in abdominal aortic aneurysms under thermal treatment, adapting those engineering tools to the peculiar geometry and physiology of the human eye.

The choice to represent the detached Descemet membrane as a flexible structure rather than a fixed boundary is what gives the study its clinical bite. Prior models of aqueous humor flow, including foundational work on fluid flow in the anterior chamber of the human eye published decades ago, captured the buoyancy-driven currents but assumed static, impermeable walls. By letting the membrane move, the new simulations capture the interplay between hemodynamics-like fluid loading and tissue compliance—precisely the interplay that governs how a detached membrane flutters against the aqueous humor, how stresses concentrate at its edges and attachments, and how different graft stiffnesses redistribute those stresses across the corneal structure. The team’s results suggest that surgeons and biomaterials scientists selecting corneal grafts for patients prone to Descemet membrane detachment could use stress predictions of this kind to weigh graft stiffness as part of the decision, even though the overall thermal environment of the chamber will remain largely unchanged.

Beyond transplantation, the model has direct relevance to thermal therapy of the eye, a class of treatments in which controlled warming is applied to manage conditions of the anterior segment. Because the simulations connect an easily controlled clinical variable—the applied temperature difference—to a measurable outcome in convective heat transfer, and because they quantify the role of iris geometry in shaping the thermal flow field, they provide a template for patient-specific treatment planning. A clinician armed with imaging of a patient’s anterior chamber geometry could, in principle, use models of this type to predict how a planned thermal protocol will distribute heat in the presence of a detached membrane, and whether the resulting stresses on the membrane fall within tolerable limits.

The work is not without its simplifications, as the authors themselves frame the study as an evaluation of corneal transplantation processes rather than a complete clinical simulator. The anterior chamber geometry is idealized, the aqueous humor is treated with standard transport properties, and the elasticity modulus range, while broad, samples the problem in parametric steps rather than matching every individual patient’s tissue. Real eyes also feature aqueous production and drainage, blinking, saccadic motion and ocular pulse effects that a steady natural-convection FSI model does not capture. Nonetheless, the paper’s central contribution—demonstrating that corneal stiffness governs membrane stress while iris geometry and thermal gradient govern heat transfer—stands as a clean separation of effects that future, more detailed models will need to reproduce.

The research was supported by the Universiti Kebangsaan Malaysia Research Grant GP-2024-K006388 and by the Deanship of Research and Graduate Studies at King Khalid University through a large Research Group Project. As computational biomechanics continues to migrate from engineering journals into clinical planning, studies like this one mark a shift toward treating the eye not as a static optical instrument but as a living, deformable, fluid-filled machine—one in which a membrane thinner than a human hair can dominate the mechanical conversation, and where the difference between a compliant and a stiff cornea may one day inform the surgeon’s graft choice.