Search Results (153)

Soil salinization has become a major global abiotic threat restricting sustainable viticulture, especially in coastal and inland saline–alkali zones. Unlike cereal crops mainly suffering from sodium toxicity, grapevine (Vitis vinifera L.) is a typical chloride-sensitive woody perennial, subjected to superimposed damages of osmotic stress, ionic imbalance and secondary oxidative injury under saline conditions which severely suppress vegetative growth and degrade berry quality. This review systematically summarizes the multi-layered physiological adaptive mechanisms of grapevine against salt stress, including ion homeostasis maintained by salt overly sensitive (SOS), Na⁺/H⁺ exchanger (NHX) and chloride channel (CLC) transporter families, active accumulation of osmoprotectants, synergistic enzymatic and non-enzymatic antioxidant systems, and phytohormone crosstalk networks formed by endogenous phytohormones (abscisic acid, ABA; jasmonic acid, JA; salicylic acid, SA; brassinosteroid, BR) and small signaling molecules. We further elaborate comprehensive molecular regulatory cascades governing salt tolerance, covering core functional genes for ion transport, master transcription factor families WRKY, MYB, APETALA2/Ethylene Response Factor (AP2/ERF), NAC, basic helix–loop–helix (bHLH) and emerging epigenetic regulatory layers mediated by deoxyribonucleic acid (DNA) methylation, microRNAs (miRNAs), long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs). In addition, we integrate four categories of field mitigation strategies for saline vineyards: germplasm improvement via salt-tolerant rootstock grafting, rhizosphere soil basal amendment, exogenous biostimulant regulation, and precision agronomic optimization. Current experimental systems do not fully recapitulate complex field combined-stress conditions, as most studies rely on laboratory single-salt stress simulation. Meanwhile, multi-omics, Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) gene editing and high-throughput phenotyping tools provide promising approaches to deepen our understanding of grape salt tolerance. This review constructs a comprehensive theoretical framework linking physiological responses, molecular regulatory networks and practical field technologies, offering systematic theoretical references and technical guidance for salt-tolerant germplasm innovation and environmentally sustainable viticulture on saline soils. Full article

Hemorrhagic shock is a leading cause of preventable death following multiple trauma, driven by a cascade of interacting cellular and molecular disturbances that extend well beyond simple volume loss. Acute blood loss initiates tissue hypoperfusion and cellular hypoxia, setting in motion the lethal triad of hypothermia, acidosis, and coagulopathy through several converging pathways: complement activation with excessive C3a and C5a production; neutrophil-mediated tissue injury; NADPH-oxidase-driven reactive oxygen species (ROS) overproduction that overwhelms superoxide dismutase defenses; mitochondrial respiratory chain impairment; dysregulation of the pro-inflammatory cytokine network; and endothelial apoptosis with degradation of the endothelial glycocalyx and disruption of interendothelial junctions, with consequent vascular hyperpermeability. These mechanisms provide the biological rationale for the resuscitation strategy. Each class of fluid acts on these pathways in a distinct way: crystalloids modulate acid–base homeostasis, chloride-mediated renal vasoconstriction, and coagulation factor activity; colloids influence oncotic pressure, endothelial integrity, and microvascular perfusion; and blood products, particularly plasma and whole blood, actively modulate mitochondrial metabolism, endothelial permeability, and pro-apoptotic signaling beyond their volume-expanding role. Translating this biology to the bedside requires a multimodal monitoring framework that converts molecular endpoints into real-time therapeutic targets, integrating lactate and base excess as markers of cellular oxygen debt, dynamic preload indices such as pulse pressure and stroke volume variation, advanced hemodynamic platforms, point-of-care ultrasonography, viscoelastic coagulation testing, and near-infrared spectroscopy of tissue oxygenation. This review synthesizes the biological basis of hemorrhagic shock and its translation into an individualized, goal-directed resuscitation strategy for the critically ill polytrauma patient. Full article

Chloride (Cl⁻) is an essential micronutrient for plants that supports multiple physiological functions throughout plant growth and development. Its effects are strongly concentration-dependent: low Cl⁻ availability promotes beneficial physiological processes, whereas excessive accumulation can induce cytotoxicity. In plants, the movement of Cl⁻ across plasma and organellar membranes is primarily mediated by three principal channel and transporter families: chloride channels (CLC), aluminum-activated malate transporters (ALMT), and slow anion channel-associated homologs (SLAC/SLAH). These families differ in gating mechanisms, ion selectivity, transport properties, and subcellular localization. This review synthesizes current knowledge of plant chloride transport proteins, with emphasis on their phylogenetic distribution, structural organization, and functional diversification. We summarize their core physiological roles in stomatal regulation, water-use efficiency, nutrient uptake, ion homeostasis, growth modulation, and abiotic stress tolerance. We also discuss how their activities are regulated by post-translational modifications, notably phosphorylation and dephosphorylation, as well as by ion concentrations, pH shifts, and phytohormone signaling. Unlike earlier reviews that primarily focused on individual transporter families or specific stress responses, this work provides an integrated framework linking structure–function relationships with regulatory networks. It also evaluates recent advances in high-resolution structural biology, electrophysiological approaches, and in vivo imaging techniques. Furthermore, we delineate current technical bottlenecks and unresolved questions, such as the molecular determinants of substrate specificity and potential cross-talk among transporter families, and propose future directions for crop improvement. By integrating structural, physiological, and regulatory perspectives, this review aims to serve as a valuable reference and stimulate interdisciplinary research on plant chloride biology. Full article

This study aimed to investigate the effects of salinity changes on serum biochemistry, hormonal profiles, splenic immune function, hepatic lipid metabolism and intestinal microbiota of the F₂ generation of Chinese sturgeon (Acipenser sinensis) under freshwater and seawater acclimation (15–23.2 psu) conditions. A 30-day indoor culture experiment showed that seawater acclimation only induced a declining trend in juvenile growth without statistical significance compared to the freshwater group (p > 0.05). The levels of triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), alkaline phosphatase (ALP) and albumin II (ALBII) in the freshwater group were markedly lower than those in the seawater group (p < 0.05), while alanine aminotransferase (ALT), aspartate aminotransferase (AST), high-density lipoprotein cholesterol (HDL-C) and total protein (TPII) showed no significant differences (p > 0.05). The serum triiodothyronine (T3) concentration was significantly higher, and chloride ion (Cl⁻) was lower in freshwater individuals (p < 0.05). Cortisol, testosterone, K⁺, Na⁺, Ca²⁺, thyroid-stimulating hormone and T4 remained unchanged between the two salinity environments (p > 0.05). In gill tissues, lipase (LPS) and fatty acid synthase (FAS) activities were lower, whereas lipoprotein lipase (LPL) activity was higher in the freshwater group (p < 0.05), and no obvious difference was observed in hepatic metabolic enzymes. The splenic complement C4 content was significantly decreased in freshwater sturgeon (p < 0.05), while splenic C3, IgM and serum immune indices showed no statistical differences. All alpha-diversity indices of intestinal microbiota were significantly higher in the seawater group (p < 0.05). At the phylum level, the intestinal flora in the seawater group was dominated by Proteobacteria (69.6%) and Fusobacteriota (14.9%), whereas Fusobacteriota accounted for 81.5% in the freshwater group. At the genus level, seawater samples exhibited richer microbial composition including Sphingomonas, Cupriavidus and Cetobacterium, while the freshwater microbiota was overwhelmingly dominated by Cetobacterium (81.5%). In conclusion, salinity significantly regulates serum biochemistry, hormone secretion, lipid metabolism, splenic immunity and intestinal microbiota of the F₂ generation of Chinese sturgeon. The freshwater environment benefits lipid metabolism, thyroid hormone levels, and growth performance, with a simplified intestinal microbial structure. Seawater acclimation maintains higher gut microbial diversity and immune homeostasis, but induces osmotic stress, restricts thyroid hormone secretion and redistributes energy supply, thereby inhibiting fish growth. This study provides a theoretical basis for salinity domestication and scientific culture management of Chinese sturgeon. Full article

In order to reveal the molecular response characteristics of different tissues of Megalobrama amblycephala under ammonia nitrogen stress, the liver, gill, muscle, kidney and brain tissues of juvenile Megalobrama amblycephala (12.05 ± 0.04 g) under 25 mg/L ammonium chloride stress were used as the research objects. The transcriptome sequencing technology was used to systematically analyze the transcriptional expression changes. A total of 204.42 Gb transcription data were obtained, and a total of 3039 DEGs were detected, of which 1331 genes were up-regulated and 1708 genes were down-regulated. Ten DEGs were randomly selected for quantitative qRT-PCR analysis, and the results confirmed that the transcriptome results were reliable. Multi-organ synergy analysis suggested that overlapping DEGs (e.g., ZNF239, DMBT1, NLRC3, MHC-I, and CCL8) may exhibit similar or opposing regulatory patterns across organs, potentially reflecting complementary and coordinated mechanisms in immune regulation, inflammatory responses, energy allocation, and detoxification strategies among organ systems. GO and KEGG pathway enrichment analysis of differentially expressed genes showed that ammonia nitrogen mainly affected immune inflammation-related processes, material transport and degradation, protein homeostasis maintenance, oxidative stress defense, membrane lipid metabolism remodeling, and energy metabolism regulation. In different tissues, genes related to specific functions are enriched according to their physiological roles: in the liver, genes related to detoxification and damage clearance are enriched; in the gill, genes related to barrier defense and antioxidant/detoxification are enriched; in the kidney, genes related to damage response and metabolic regulation are enriched; in the brain, genes related to membrane lipid homeostasis and protective stress are enriched; and in the muscle, genes related to energy metabolism and structural function adjustment are enriched. This study elucidated the multi-tissue response characteristics of Megalobrama amblycephala under ammonia nitrogen stress at the transcriptome level, providing fundamental data and references for further clarifying the mechanisms of ammonia nitrogen toxicity in fish and screening stress-responsive marker genes. Full article

Major depressive disorder (MDD) remains a leading cause of disability; however, monoaminergic models do not fully explain delayed treatment onset, incomplete remission, or rapid responses to glutamatergic interventions. In this study, we proposed a system-level ionic homeostasis framework for MDD. In this model, genetic susceptibility, chronic stress, metabolic burden, and neuroinflammation converge in neuronal and glial ion-channel systems, disrupting calcium, potassium, chloride, and purinergic homeostasis. These disturbances alter intrinsic excitability, synaptic integration, inhibitory tone, glial buffering, and neuron–glia signaling, thereby promoting excitation–inhibition imbalance, impaired plasticity, and corticolimbic network instability. We reviewed the evidence implicating the CACNA1C/Cav1.2, TREK-1, KCNQ, NKCC1/KCC2, HCN, transient receptor potential/acid-sensing ion channels, and glial mediators, including P2X7R, Kir4.1, and AQP4. We also discuss how ketamine-related mechanisms, chloride-restoring strategies, anti-inflammatory ion channel targeting, neuromodulation, EEG biomarkers, and AI/multiomics approaches support mechanism-informed precision therapeutics. MDD could be conceptualized as a distributed failure of ionic homeostasis that links neuroinflammation, E/I imbalance, network instability, and impaired adaptive plasticity. Full article

The protective effect of Compound terminalia chebula extract (HL) against colonic injury induced by Porcine epidemic diarrhea virus (PEDV) infection in neonatal piglets remains unclear. This study aimed to evaluate the mitigating effects of HL on PEDV-induced colonic injury and elucidate the underlying mechanisms. Eighteen 7-day-old Duroc × Landrace × Large White piglets (2.58 ± 0.05 kg) were randomly assigned to three groups (n = 6/group): CON (blank control), PEDV (infected), and HL + PEDV (HL-supplemented + infected). The 11-day trial included 3 days of acclimatization (days 0–3) and an 8-day experimental period (days 4–11). HL (10 mg/kg BW) was orally administered daily to the HL + PEDV group. On day 8, PEDV and HL + PEDV groups were challenged with 3 mL PEDV (3 × 10⁶ TCID₅₀/mL), while CON received Dulbecco’s Modified Eagle Medium (DMEM). All piglets were euthanized on day 11 for colonic tissue collection. Results indicated that PEDV infection induced colonic injury, manifested by a significant increase in crypt depth and disruption of intestinal homeostasis. This was evidenced by impaired barrier integrity (upregulation of matrix metalloproteinase-7 gene [MMP7] and matrix metalloproteinase 13 gene [MMP13], mucus disorganization (elevation of mucin 5AC gene [MUC5AC]), oxidative stress (reduced catalase [CAT] activity and increased malondialdehyde [MDA] levels in serum and colon), and inflammation (upregulation of regenerative islet-derived protein 3γ gene [REG3G], S100 calcium-binding protein A8/A9 gene [S100A8/A9], and interleukin-1β gene [IL-1β]). Additionally, PEDV impaired colonic ion transport by downregulating calcium channel genes (Transient Receptor Potential Cation Channel Subfamily V Member 6 gene [TRPV6], Transient Receptor Potential Cation Channel Subfamily M Member 6 gene [TRPM6]). Notably, HL supplementation effectively reversed these adverse effects. HL restored colonic morphology, increased CAT activity, reduced MDA accumulation, and suppressed inflammatory gene expression. Furthermore, HL modulated the expression of genes involved in water and ion transport upregulating Aquaporin 7 gene (AQP7), Chloride Channel Accessory 4 gene (CLCA4), Sodium-Hydrogen Exchanger 3 gene (NHE3), Transient Receptor Potential Vanilloid 6 (TRPV6), and Transient Receptor Potential Melastatin 6 gene (TRPM6) and significantly inhibited PEDV replication, as indicated by the downregulation of the transcription levels of PEDV membranegene (M), nucleocapsid gene (N), and spike gene (S). Taken together, HL alleviates PEDV-triggered colonic tissue damage in suckling piglets via improving colonic antioxidant capacity, mitigating inflammatory response, partially regulating intestinal barrier and ion/water transport-related genes, and downregulating the transcription of PEDV structural genes at molecular and histological levels. Full article

Drought is one of the major abiotic stresses limiting soybean production, and its detrimental effects are jointly influenced by stress intensity, duration, and cultivation conditions. To investigate the morphological and physiological regulatory mechanisms by which mepiquat chloride (DPC) alleviates drought stress at the soybean seedling stage, this study used the drought-tolerant soybean cultivar Heinong 44 (H-44) and the drought-sensitive cultivar Heinong 65 (H-65) as experimental materials. Osmotic stress was simulated with 10% PEG-6000 at the V2 stage, and the effects of foliar application of different DPC concentrations (125–500 mg/L) on soybean morphology, biomass allocation, antioxidant systems, and osmotic adjustment capacity were systematically analyzed. The results showed that drought stress significantly inhibited the growth of both soybean cultivars and induced severe oxidative damage. Appropriate DPC concentrations moderately restricted shoot growth to reduce transpiration area while promoting root growth to enhance water acquisition capacity. The optimal DPC concentrations for alleviating drought stress were 200 mg/L for H-44 and 275 mg/L for H-65. Allometric growth analysis indicated that drought disrupted the original root–shoot growth pattern, whereas appropriate DPC concentrations significantly promoted dry matter accumulation in drought-stressed plants and improved root–shoot growth coordination. However, an excessive concentration of DPC (500 mg/L) caused an abnormal deviation in the growth trajectory. In addition, appropriate DPC concentrations synergistically enhanced the activities of superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), and ascorbate peroxidase (APX) in leaves and roots under drought conditions; promoted the accumulation of proline (Pro), soluble sugars (Ss), and soluble proteins (Sp); effectively reduced the contents of malondialdehyde (MDA) and hydrogen peroxide (H₂O₂); and protected cell membrane stability. In conclusion, DPC synergistically enhances drought resistance in soybean by reshaping the root–shoot allometric growth configuration and systematically activating physiological defense networks, providing a theoretical basis for chemically regulated cultivation of soybean under stress conditions. Full article

Background: Systemic arterial hypertension (SAH) induced by Nω-nitro-L-arginine methyl ester (L-NAME) is a well-established model characterized by nitric oxide (NO^●) synthase inhibition and vascular dysfunction. The transient receptor potential vanilloid 1 (TRPV1) regulates Ca²⁺ flux and may contribute to mitochondrial homeostasis. We hypothesized that TRPV1 activation modulates mitochondria function and attenuates cardiac damage during SAH. Methods: Hypertension was induced in Wistar rats by administration of L-NAME (200 mg/L) for 40 days. During the last four days, hypertensive animals received capsaicin (5 mg/kg/day), capsazepine (6 mg/kg/day), or their combination. Cardiac function was evaluated in isolated hearts using the Langendorff perfusion system. Myocardial tissue viability was assessed by triphenyltetrazolium chloride (TTC) staining, and mitochondrial function was evaluated by measuring respiratory control and apoptosis-related proteins. Results: Capsaicin treatment was associated with significant cardioprotective effects in hypertensive rats. Although the findings are consistent with a role of TRPV1 activation in mediating these effects, the partial protection observed with capsazepine suggests that TRPV1-independent mechanisms may also contribute. Conclusions: TRPV1 activation contributes to cardioprotection in SAH, likely through preservation of mitochondrial function and redox balance. However, additional mechanisms beyond TRPV1 modulation may also participate in the observed protective effects. Further studies—including direct assessment of mitochondrial Ca²⁺ flux and the use of more selective or genetic approaches—are currently underway to clarify the underlying mechanisms. Full article

Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) dysfunction is increasingly recognized as a key contributor to a broad spectrum of human diseases beyond classical cystic fibrosis (CF). CFTR is a cAMP-regulated chloride and bicarbonate ion channel expressed in both epithelial and non-epithelial tissues, where it regulates ion homeostasis, mucosal hydration, and cellular signaling. Both inherited CFTR mutations and acquired dysfunction resulting from environmental or inflammatory factors can disrupt these physiological processes and drive disease progression. Current evidence linking CFTR dysregulation to respiratory diseases, such as cystic fibrosis, chronic obstructive pulmonary disease (COPD), asthma, and HIV-associated airway disease, as well as cardiovascular, renal, neurological diseases, and cancer, is comprehensively discussed. Mechanistically, impaired CFTR function promotes oxidative stress, chronic inflammation, epithelial barrier dysfunction, altered mucociliary clearance, and dysregulation of signaling pathways, including NF-κB, TGF-β, PI3K/Akt, MAPK, and Wnt/β-catenin. In the context of HIV infection and cigarette smoke exposure, CFTR suppression is mediated in part by TGF-β signaling and miRNA-dependent mechanisms, resulting in compromised airway defense and increased susceptibility to pulmonary complications. Recent studies further demonstrate that CFTR dysregulation alters the expression of genes involved in fibrosis, inflammation, angiogenesis, and epithelial–mesenchymal transition (EMT). Notably, CFTR may act as either a tumor suppressor or a context-dependent oncogene, depending on tissue type and signaling milieu, highlighting its complex role in cancer biology. Advances in CFTR-targeted therapies, including potentiators, correctors, gene therapy, and combination approaches, have markedly improved outcomes in CF and may offer therapeutic potential for diseases associated with acquired CFTR dysfunction. We summarize the systemic consequences of CFTR dysregulation and the need for further mechanistic and translational research to clarify its role across diverse human diseases. Full article

Background: The regulation of inorganic phosphate (Pi) homeostasis is predominantly mediated by the Pi transporters belonging to the SLC34 and SLC20 families of solute carriers. However, not all Pi handling can be explained by these transporters. In this study, we sought to identify novel Pi transporters in accordance with prior findings on inhibition patterns. Methods: We have performed a functional screening of new Pi carriers using the Xenopus laevis oocyte expression system, focusing on the SLC26 family, and corroboration in cell culture. Results: Both SLC26A7 and SLC26A9 have been shown to express sodium-activated Pi uptakes with approximately 200 µmol/L Pi affinity. In both cases, Pi transport is inhibited by increasing pH and by phosphonoformate, arsenate, bicarbonate, sulfate, the chloride channel inhibitor 5-nitro-2-[(3-phenylpropyl)amino]-benzoate, and several transport site and translocation inhibitors of bicarbonate exchangers. In addition, the CFTR inhibitor GlyH-101 and the SLC4 inhibitors DIDS, SITS, and phloretin exhibited partial inhibition of SLC26A9-mediated Pi uptake. The endogenous expressions of both SLC26A7 and SLC26A9 in the renal cell lines LLC-PK1 and MDCK were primarily intracellular, colocalizing with endosomes, lysosomes, and the trans-Golgi network markers. Conversely, plasma membrane expression was found to be minimal. Pi transport in MDCK cells was sodium-independent, but when either SLC26A7 or SLC26A9 was overexpressed, sodium-activated Pi uptake was observed, along with increased expressions of SLC26A7 or SLC26A9 in the plasma membrane. Conclusions: Sodium-activated Pi transport is a novel function of the SLC26A7 and SLC26A9 multifunctional anion transporters. Further research is necessary to ascertain the relevance to Pi homeostasis in vivo. Full article

Soil salinity is a major environmental constraint affecting avocado (Persea americana Mill.) productivity. In this study, we evaluate the physio-morphological and molecular responses of two avocado varieties, drymifolia (sensitive) and americana (tolerant), subjected to increasing NaCl concentrations for 60 days. Our results reveal distinct adaptive strategies. While salinity reduced total biomass in both genotypes, var. americana exhibited superior resilience, characterized by preferential biomass allocation to the root system. Ion analysis demonstrated that tolerance was not mediated by K⁺ homeostasis, but rather by the differential management of toxic ions. var. americana effectively sequestered chloride Cl⁻ in the roots, whereas var. drymifolia exhibited a breakdown of the exclusion mechanism at 60 mM NaCl, with shoot Cl⁻ concentrations exceeding those of the root, leading to severe toxicity. At the molecular level, qPCR analysis of the Na⁺ transporters PaHKT1 and PaSOS1 showed no expression pattern correlated with salt stress. Bioinformatic assessment revealed significant structural divergences and a lack of conserved functional domains in these proteins. These findings challenge the applicability of the classical sodium-exclusion model (typical of Liliopsida and Magnoliopsida) to avocado. We conclude that salt tolerance in this Lauraceae species is primarily driven by root-mediated Cl⁻ exclusion rather than canonical Na⁺ transport pathways. Full article

Purpose: A high-salt extracellular environment promotes fibrosis in multiple organs by inducing oxidative stress, fibroblast activation, and extracellular matrix remodeling. In the lung, sodium accumulation may result from impaired epithelial ion transport. Transforming growth factor-β1 (TGF-β1), a key profibrotic cytokine, downregulates epithelial sodium and chloride channels, promoting sodium retention and fibrotic remodeling. This study investigated whether antifibrotic drugs can prevent TGF-β1-induced suppression of sodium channel expression in the lung epithelium. Methods: Human A549 alveolar epithelial cells and primary alveolar epithelial cells were cultured with or without TGF-β1 in the presence or absence of nintedanib or pirfenidone. Expression of epithelial sodium channel (ENaC) subunits (SCNN1A, SCNN1B, SCNN1G, SCNN1D) and CFTR was analyzed. In vivo, lung tissues from TGF-β1 transgenic mice and wild-type controls were examined following intranasal administration of pirfenidone. Results: TGF-β1 markedly reduced the expression of all ENaC subunits and CFTR in vitro. Nintedanib prevented suppression of SCNN1A, SCNN1D, and SCNN1G, whereas pirfenidone prevented suppression of SCNN1A, SCNN1B, and SCNN1G. In TGF-β1 transgenic mice, Scnn1a, Scnn1b, and Scnn1g expression was significantly decreased compared with wild-type controls. Pirfenidone administration dose-dependently restored expression of these ENaC subunits in vivo. Conclusions: Antifibrotic drugs partially prevent TGF-β1-induced suppression of epithelial sodium channels, preserving epithelial ion homeostasis. Restoration of ENaC expression may represent a novel mechanism by which antifibrotic therapy mitigates sodium-associated lung fibrosis. Full article

Citrus production is increasingly constrained worldwide by rising soil salinity, particularly in arid and semi-arid regions. In Tunisia, the expansion of saline soils represents a major abiotic stress limiting orchard productivity. The identification of salt-tolerant rootstocks has therefore become a priority, especially as alternatives to sour orange (SO, Citrus aurantium L.), which is highly susceptible to Citrus tristeza virus. In recent years, several outbreaks of the disease have been reported in the Cap Bon citrus-growing region, posing an imminent threat to the sustainability of citrus production in Tunisia. This study evaluated the salt tolerance of commercial cultivars (HER, MAR, WN, NH) grafted onto Citrus volkameriana Ten. & Pasq. (CV, Citrus aurantium × Citrus limon (L.) Burm.f.) and three Poncirus trifoliata hybrids (CC, C35, CTR) under irrigation water salinity ranging from 1.1 to 4.1 mS/cm and soil salinity between 1.8 and 3.8 mS/cm. Data were collected between 2020 and 2021 in five young citrus orchards (KHB, OSN, BKN, BSJ, CHK) located in the main citrus-producing region of Tunisia, with key physiological measurements conducted during the high-evaporation period. Salinity increased across most sites during summer 2021, affecting ion homeostasis, Na⁺/K⁺ selectivity, stomatal traits, photosynthetic performance, and growth. The highest leaf Cl⁻ concentration (0.4 meq g⁻¹ dry weight) was recorded in the sensitive HER/CC combination at the OSN site. Increased salinity at OSN was associated with a 0.86% reduction in canopy growth compared to BSJ. Rootstock tolerance was strongly linked to the ability to restrict Cl⁻ accumulation in leaf tissues. Under higher salinity conditions, CV showed superior performance and represents a suitable alternative to SO. Full article

Mucins are highly glycosylated proteins that form the structural basis of mucus and represent a key component of innate immunity at mucosal surfaces, particularly in the respiratory tract. Beyond their mechanical barrier function, mucins actively participate in pathogen trapping, regulation of mucociliary clearance, modulation of inflammatory responses, and maintenance of epithelial homeostasis. Dysregulation of mucin synthesis, composition, or transport contributes to mucus hypersecretion, impaired airway clearance, and chronic inflammation in respiratory diseases such as asthma, chronic obstructive pulmonary disease, and cystic fibrosis. This review summarizes current insights into mucin biology, including their biosynthesis, structure, classification, and regulation, with emphasis on the gel-forming mucins MUC5AC and MUC5B. The role of mucins in mechanical protection, host–pathogen interactions, control of inflammation, and coordination of innate immune responses is reviewed. Attention is given to the interplay between mucins, immune cells, and microbial communities in maintaining airway barrier integrity. The article further examines mucoactive therapeutic strategies aimed at restoring mucus barrier function. Expectorants, mucolytics, mucoregulators, and mucokinetic agents are reviewed with respect to their mechanisms of action and clinical relevance. Established drugs, including N-acetylcysteine, carbocysteine, dornase alfa, ambroxol, and hypertonic solutions, are considered alongside emerging molecular targets such as NF-κB-dependent regulation of mucin expression, calcium-activated chloride channels, MARCKS-mediated mucin exocytosis, purinergic signaling pathways, and NO/cGMP signaling. Non-pharmacological approaches, including airway clearance techniques and respiratory rehabilitation, are covered concisely. Conclusions: Overall, this review highlights mucins as dynamic regulators of innate immunity and underscores the need for mechanism-based, personalized mucoactive therapies to improve outcomes in chronic inflammatory airway diseases. Full article