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21 pages, 2629 KB  
Article
Evaluating Chlorella vulgaris as a Biostimulant for Salt and Heat Stress Tolerance in Chenopodium quinoa
by Lucia Giorgetti, Andrea Melchiorre, Laryssa Peres Fabbri, Morena Gabriele and Lorenza Bellani
Environments 2026, 13(4), 182; https://doi.org/10.3390/environments13040182 (registering DOI) - 26 Mar 2026
Abstract
Recent climate changes worldwide have negatively impacted crop yields, highlighting the urgent need to develop new cultivation strategies to counteract this phenomenon. Our study aimed to analyze the effects of saline (0 mM, 100 mM, 200 mM, and 300 mM NaCl) and heat [...] Read more.
Recent climate changes worldwide have negatively impacted crop yields, highlighting the urgent need to develop new cultivation strategies to counteract this phenomenon. Our study aimed to analyze the effects of saline (0 mM, 100 mM, 200 mM, and 300 mM NaCl) and heat stress (24 °C and 32 °C) on the physiological parameters of Chenopodium quinoa variety “Regalona,” evaluating the efficacy of the microalgal biostimulant Chlorella vulgaris-like extract (0%, 0.025% and 0.05%). Sprouts grown under these different conditions were assessed for antioxidant content, antioxidant activity, reactive oxygen species, and photosynthetic pigments. The analyses did not reveal significant effects of the two microalgal concentrations on germination percentage or sprout length across the various temperature and salinity conditions. However, antioxidant activity was increased in many experimental trials, especially when the microalgae were combined with salt stress, with the higher biostimulant concentration showing more pronounced effects. Conversely, a temperature of 32 °C negatively impacted the parameters measured. These findings provide a basis for further research aimed at enhancing the antioxidant and nutraceutical properties of plants valuable for human nutrition. Full article
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22 pages, 493 KB  
Review
Oxidative Stress in Multiple Myeloma: Pathogenic Mechanisms, Biomarkers, and Redox-Targeted Therapeutic Strategies
by Rafał Bilski, Daria Kupczyk, Karolina Kaczorowska-Bilska, Halina Tkaczenko, Natalia Kurhaluk, Tomasz Kosmalski, Artur Słomka and Renata Studzińska
Int. J. Mol. Sci. 2026, 27(7), 3001; https://doi.org/10.3390/ijms27073001 (registering DOI) - 25 Mar 2026
Abstract
Multiple myeloma (MM) is an incurable plasma cell malignancy characterized by high metabolic activity, chronic endoplasmic reticulum stress, and persistent redox imbalance. Excessive immunoglobulin synthesis and adaptation to the hypoxic bone marrow microenvironment lead to sustained production of reactive oxygen species (ROS). Their [...] Read more.
Multiple myeloma (MM) is an incurable plasma cell malignancy characterized by high metabolic activity, chronic endoplasmic reticulum stress, and persistent redox imbalance. Excessive immunoglobulin synthesis and adaptation to the hypoxic bone marrow microenvironment lead to sustained production of reactive oxygen species (ROS). Their excessive accumulation promotes genomic instability, disease progression, osteolytic bone disease, and resistance to therapy. Paradoxically, MM cells adapt to oxidative stress by activating antioxidant and metabolic defense mechanisms, including Nuclear factor erythroid 2-related factor 2 (NRF2)- and Heme Oxygenase 1 (HMOX1)-dependent pathways, metabolic reprogramming, and overexpression of ROS-scavenging enzymes such as peroxiredoxin 6 (PRDX6), allowing survival at the threshold of oxidative toxicity. Evidence indicates that biomarkers of oxidative stress—such as lipid and protein oxidation products, antioxidant enzyme activity, and the Oxidative Stress Score—correlate with disease stage, prognosis, and treatment response. Redox-modulating therapeutic strategies, including pharmacological ROS induction, inhibition of antioxidant defenses, and the use of natural pro-oxidant compounds, are emerging as promising adjuncts to standard MM therapies. Recent studies also highlight the gut microbiota as an indirect regulator of oxidative balance, immune modulation, and metabolic homeostasis in MM. This review summarizes current knowledge on oxidative stress in multiple myeloma, emphasizing its role in pathogenesis, drug resistance, biomarker development, and emerging therapeutic and supportive strategies. Full article
23 pages, 53767 KB  
Article
BNIP3/BNIP3L-Dependent Mitophagy Protects Against Hippocampal Neuronal Damage and Apoptosis in a Model of Vascular Dementia
by Yujiao Wang, Daojun Xie, Shijia Ma, Yuhe Wang, Chengcheng Zhang and Zhuyue Chen
Cells 2026, 15(7), 585; https://doi.org/10.3390/cells15070585 (registering DOI) - 25 Mar 2026
Abstract
Mitophagy serves as an essential quality control mechanism that maintains mitochondrial homeostasis through selective autophagic clearance of damaged organelles. Vascular dementia (VD) has been increasingly associated with mitophagy dysregulation in recent studies. However, the precise molecular mechanisms underlying mitophagy’s involvement in VD pathogenesis [...] Read more.
Mitophagy serves as an essential quality control mechanism that maintains mitochondrial homeostasis through selective autophagic clearance of damaged organelles. Vascular dementia (VD) has been increasingly associated with mitophagy dysregulation in recent studies. However, the precise molecular mechanisms underlying mitophagy’s involvement in VD pathogenesis remain poorly characterized. To elucidate the role of mitophagy in VD, we systematically examined the expression of key mitophagy pathways in hippocampal neurons of bilateral common carotid artery occlusion (BCCAO) rats and in oxygen–glucose deprivation (OGD)-treated HT22 cells. Intriguingly, under autophagy-deficient conditions, both BNIP3 and BNIP3L were markedly downregulated, whereas FUNDC1 expression increased; PINK1/Parkin levels remained unaltered. To further dissect the functional contributions of BNIP3 and BNIP3L, we administered the mitochondrial fission inhibitor Mdivi-1 to BCCAO model rats. Histopathological analysis revealed pronounced neuronal damage and apoptosis in the hippocampal region, which was further exacerbated upon Mdivi-1 treatment. In vitro, BNIP3 silencing significantly compromised cell viability, elevated reactive oxygen species (ROS) accumulation, disrupted mitochondrial membrane potential (ΔΨm), suppressed mitophagy, and increased apoptotic rates. Conversely, BNIP3 overexpression reversed these detrimental effects. Notably, treatment with the autophagy inhibitor 3-methyladenine (3-MA) diminished LC3B-Tomm20 colocalization and intensified apoptosis, reinforcing the critical role of BNIP3-mediated mitophagy in neuronal survival. Similarly, BNIP3L overexpression enhanced cell viability, attenuated ROS production, restored ΔΨm, and mitigated apoptosis, while 3-MA treatment again impaired mitophagic flux and worsened cell death. Collectively, these findings underscore the critical and distinct roles of BNIP3 and BNIP3L in maintaining mitochondrial homeostasis and neuronal survival under ischemic conditions. Full article
(This article belongs to the Special Issue Autophagy-Related Proteins in Stress Responses)
27 pages, 2362 KB  
Article
Source-Specific Photobiomodulation Regulates Mitochondrial Bioenergetics, Redox Signaling, and Functional Outputs in C2C12 Myoblasts Across Replicative Aging
by Ana Elena Aviña, Nguyen Le Thanh Hang, Che-Yi Chang, Yi-Fan Chen, Yun Yen, Xavier Pei-Chun Wong, Aline Yen Ling Wang, Cheng-Jen Chang and Tzu-Sen Yang
Int. J. Mol. Sci. 2026, 27(7), 2999; https://doi.org/10.3390/ijms27072999 (registering DOI) - 25 Mar 2026
Abstract
Age-related muscle decline is associated with impaired mitochondrial bioenergetics, altered redox signaling, and reduced myogenic capacity, yet how photobiomodulation (PBM) source characteristics shape these processes under replicative aging remains unclear. Here, we investigated source-specific PBM responses in C2C12 myoblasts using a 660 nm [...] Read more.
Age-related muscle decline is associated with impaired mitochondrial bioenergetics, altered redox signaling, and reduced myogenic capacity, yet how photobiomodulation (PBM) source characteristics shape these processes under replicative aging remains unclear. Here, we investigated source-specific PBM responses in C2C12 myoblasts using a 660 nm light-emitting diode (LED) and an 830 nm near-infrared (NIR) laser across fluence ranges and replicative stages. Single-cell screening performed at passage 25 identified 5 J/cm2 as the optimal fluence for both sources, producing biphasic increases in mitochondrial membrane potential and ROS. Population-level assays in young (≤5 passages) and old (≥30 passages) cells revealed divergent downstream outcomes. LED irradiation elicited stronger metabolic activation and ATP production, particularly in aged cells, whereas NIR irradiation robustly enhanced myogenic fusion in both age groups and partially rescued differentiation deficits in aged myoblasts. Bulk ROS increased significantly after PBM independent of source, while extracellular vesicle release displayed age-dependent source sensitivity, with NIR favoring canonical small EV populations in young cells and LED inducing greater particle release in aged cells. Together, these findings demonstrate that PBM engages conserved mitochondrial signaling while source-specific delivery and wavelength differentially direct metabolic, paracrine, and myogenic outputs under replicative aging conditions. Full article
(This article belongs to the Special Issue Advances in Photobiomodulation Therapy)
18 pages, 5099 KB  
Article
Biochar-Stabilized Tea Tree Oil in Chitosan Membranes for Sustainable Antimicrobial Packaging
by Kang Zhang, Jing Sun, Peiqin Cao, Yixuan He, Yixiu Wang and Hongxu Zhu
Molecules 2026, 31(7), 1079; https://doi.org/10.3390/molecules31071079 - 25 Mar 2026
Abstract
This study developed an active packaging material by incorporating tea tree oil (TTO)-loaded lotus stalk biochar (BC@TTO) into a chitosan (CS) matrix. Biochar was prepared from lotus stalks via pyrolysis at 600 °C and characterized, revealing a mesoporous structure with a specific surface [...] Read more.
This study developed an active packaging material by incorporating tea tree oil (TTO)-loaded lotus stalk biochar (BC@TTO) into a chitosan (CS) matrix. Biochar was prepared from lotus stalks via pyrolysis at 600 °C and characterized, revealing a mesoporous structure with a specific surface area of 35.9 m2/g. Adsorption studies demonstrated that BC exhibited high affinity for TTO, following pseudo-first-order kinetics and the Langmuir isotherm model, with a maximum adsorption capacity of 295.6 mg/g. Chitosan-based composite membranes with varying BC@TTO contents (1–7 wt%) were fabricated by solution casting. The incorporation of BC@TTO significantly enhanced the tensile strength, elongation at break, barrier properties (water vapor and oxygen), and antioxidant/antibacterial activities of the membranes, with optimal performance observed at 3 wt% loading. However, higher loadings led to filler aggregation, reduced transparency, and compromised mechanical properties. In vitro release studies indicated that TTO release followed the Avrami model, suggesting a diffusion-controlled mechanism. Preservation tests on blueberries showed that the CS-3BC@TTO membrane effectively reduced weight loss and maintained fruit quality during storage. This work presents a promising strategy for designing bioactive packaging materials with sustained release functionality for food preservation applications. Full article
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20 pages, 336 KB  
Article
Maternal Omega-3 PUFA Supplementation and Mitochondrial Function in a Newborn Piglet Model: A Preliminary Investigation
by Paweł Kowalczyk, Monika Sobol, Ewa Święch, Anna Tuśnio, Marcin Barszcz, Jarosław Woliński, Joanna Makulska, Andrzej Węglarz and Grzegorz Skiba
Int. J. Mol. Sci. 2026, 27(7), 2995; https://doi.org/10.3390/ijms27072995 - 25 Mar 2026
Abstract
Maternal nutrition during pregnancy plays a crucial role in fetal development and metabolic programming. Long-chain omega-3 polyunsaturated fatty acids (LC-PUFA n-3), particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are known to influence mitochondrial function and cellular energy metabolism. The present preliminary study [...] Read more.
Maternal nutrition during pregnancy plays a crucial role in fetal development and metabolic programming. Long-chain omega-3 polyunsaturated fatty acids (LC-PUFA n-3), particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are known to influence mitochondrial function and cellular energy metabolism. The present preliminary study aimed to evaluate the effects of maternal omega-3 supplementation on mitochondrial bioenergetics in neonatal piglets. Pregnant sows were supplemented with either fish oil or algal oil rich in LC-PUFA n-3 (long-chain omega-3 polyunsaturated fatty acids) throughout gestation. Liver samples were collected from newborn piglets immediately after birth, and mitochondrial respiratory parameters, oxygen consumption rates, and selected oxidative stress markers were analyzed. The results indicated that maternal omega-3 supplementation was associated with improved mitochondrial respiratory parameters and enhanced oxidative phosphorylation efficiency in neonatal liver tissue. Both fish oil and algal oil supplementation showed similar trends in improving mitochondrial bioenergetic function. Although the study was exploratory and conducted on a limited number of animals, the findings suggest that maternal intake of LC-PUFA n-3 may influence mitochondrial metabolism in offspring. Further studies with larger experimental groups are required to confirm these observations and to better understand the mechanisms underlying these effects. Full article
27 pages, 5684 KB  
Article
Carbon Dots–TiO2 Hybrid Nanomaterials with Enhanced Photochemical Properties and Photodynamic Therapy Activity
by Alexandra Karagianni, Adamantia Zourou, Afroditi Ntziouni, Conghang Qu, Mauricio Terrones, Christos Argirusis, Eleni Alexandratou and Konstantinos V. Kordatos
Processes 2026, 14(7), 1048; https://doi.org/10.3390/pr14071048 - 25 Mar 2026
Abstract
Photodynamic therapy (PDT) is a promising cancer treatment employing photo-induced reactive oxygen species (ROS) generation by a photosensitizer (PS). Titanium dioxide (TiO2) is a potential PS due to its superb photocatalytic features and biocompatibility. However, its clinical potential is restricted by [...] Read more.
Photodynamic therapy (PDT) is a promising cancer treatment employing photo-induced reactive oxygen species (ROS) generation by a photosensitizer (PS). Titanium dioxide (TiO2) is a potential PS due to its superb photocatalytic features and biocompatibility. However, its clinical potential is restricted by its predominant ultraviolet (UV) absorption. To address this limitation, this work introduces TiO2/carbon dots (CDs) nanohybrid materials for improving the photophysical properties of TiO2 and its photodynamic performance. TiO2 and CDs were synthesized through wet chemical and hydrothermal techniques, and subsequently combined via a facile ex situ solvothermal process to produce hybrid materials containing 1–50% w/w CDs. The materials were characterized using XRD, Raman, TEM, FT-IR, zeta potential, TGA, UV-Vis and PL. PDT studies on A431 skin cancer cells indicated improved photosensitizing ability of TiO2/CDs, with TiO2/CDs (10%) inducing 47% cell toxicity, versus 20% for TiO2 after 10 min of red-light irradiation (661 nm, 18 mW/cm2, 12.96 J/cm2). Intracellular localization studies revealed enhanced cellular uptake of TiO2/CDs (10%), compared with TiO2. In vitro studies on 3T3 healthy fibroblasts confirmed PSs’ safety both with and without light. Overall, this study elucidates the key role of CDs in the photophysical and photodynamic behavior of TiO2-based systems, providing design guidelines for the next-generation inorganic PSs. Full article
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55 pages, 1592 KB  
Review
Oxidative Stress-Driven Mechanisms and Biomarkers of Drug-Induced Nephrotoxicity: Translational Insights and Therapeutic Implications
by Rizwan Ahamad, Nida Mubin, Mohammed Alnukhali, Mohd Akhtar, Mohd Aqil, Mohd Mujeeb and Anis Ahmad
Antioxidants 2026, 15(4), 412; https://doi.org/10.3390/antiox15040412 - 25 Mar 2026
Abstract
Drug-induced kidney injury remains a major clinical challenge associated with diverse therapeutic agents and is an important cause of acute kidney injury, chronic renal dysfunction, and treatment-related morbidity. Growing evidence indicates that nephrotoxicity caused by anticancer, immunosuppressive, and anti-infective drugs is strongly driven [...] Read more.
Drug-induced kidney injury remains a major clinical challenge associated with diverse therapeutic agents and is an important cause of acute kidney injury, chronic renal dysfunction, and treatment-related morbidity. Growing evidence indicates that nephrotoxicity caused by anticancer, immunosuppressive, and anti-infective drugs is strongly driven by oxidative stress and redox homeostasis disruption. Excessive production of reactive oxygen species (ROS) in renal tubular cells overwhelms endogenous antioxidant defenses and triggers mitochondrial dysfunction, inflammatory signaling, and activation of stress-responsive pathways that culminate in tubular injury and renal functional decline. These processes promote apoptosis, necrosis, microvascular injury, and a reduction in the glomerular filtration rate, while dysregulation of redox-sensitive pathways involved in cell survival and repair further heightens renal vulnerability. This review summarizes current mechanistic insights into oxidative stress-mediated pathways of drug-induced nephrotoxicity, with emphasis on their translational relevance. In addition, it discusses emerging biomarkers for early detection and highlights recent advances in antioxidant-based and redox-modulating strategies that may help prevent renal injury and preserve kidney function. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Kidney Diseases)
22 pages, 3717 KB  
Article
Controlling Oxygen Vacancies in BiFeO3 Thin Films via Pyrolysis Temperature and O2 Annealing
by Saulo P. Reis, Marco Antonio M. Teixeira, Fernando B. Minussi, Maria Jesus Hortigüela, Gonzalo Otero-Irurueta, Leandro Bufaiçal and Eudes B. Araújo
Nanomaterials 2026, 16(7), 395; https://doi.org/10.3390/nano16070395 - 25 Mar 2026
Abstract
Bismuth ferrite (BiFeO3) is a promising material for developing the next generation of multifunctional electronic devices. However, the production of high-quality BiFeO3 thin films is compromised by the tendency for structural and electronic defects to form during synthesis, which degrades [...] Read more.
Bismuth ferrite (BiFeO3) is a promising material for developing the next generation of multifunctional electronic devices. However, the production of high-quality BiFeO3 thin films is compromised by the tendency for structural and electronic defects to form during synthesis, which degrades their functional properties. In this work, BiFeO3 thin films were prepared by chemical solution deposition to determine optimal conditions for minimizing oxygen vacancies and to evaluate the impact of these point defects on their physical properties. The films were pyrolyzed at 300 °C for 60 min and 360 °C for 10 min, and crystallized in air and in an O2 atmosphere, at 600 °C and 640 °C for 40 min. High oxygen vacancies were observed in films prepared at low pyrolysis temperatures and crystallized in air, whereas oxygen vacancies were minimized in the film pyrolyzed and crystallized at high temperatures in an O2 atmosphere. The oxygen vacancies markedly affected the films’ physical properties, leading to increased dielectric loss, dielectric dispersion, dc conductivity, and leakage current, with consequent degradation of photovoltaic and magnetic performance. These findings highlight the critical importance of controlling synthesis parameters to suppress oxygen vacancy formation and achieve high-quality BiFeO3 thin films. Full article
(This article belongs to the Section Synthesis, Interfaces and Nanostructures)
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14 pages, 2389 KB  
Article
Seasonal Dynamics of Eukaryotic Microbial Communities in the Mussel (Mytilus coruscus) Raft-Culture Area of Gouqi Island
by Yaodong He, Zhengwei Peng, Fenglin Wang, Peitao Liu, Shirui Mu, Yaqiong Wang and Xiumei Zhang
Microbiol. Res. 2026, 17(4), 66; https://doi.org/10.3390/microbiolres17040066 - 25 Mar 2026
Abstract
Eukaryotic microorganisms, including microalgae, protists, fungi, and micro-metazoans, act as drivers of energy flow and nutrient cycling, collectively forming the microbial food loop, and also serve as important indicators of environmental health. To investigate the seasonal variation in eukaryotic microorganisms in a mussel [...] Read more.
Eukaryotic microorganisms, including microalgae, protists, fungi, and micro-metazoans, act as drivers of energy flow and nutrient cycling, collectively forming the microbial food loop, and also serve as important indicators of environmental health. To investigate the seasonal variation in eukaryotic microorganisms in a mussel farming area, a total of 96 seawater samples were collected from surface and bottom layers of water across different seasons. High-throughput sequencing of the 18S rRNA gene was employed to characterize shifts in microbial community structure and identify key influencing factors. Our results indicated significant seasonal differences in eukaryotic microbial communities between surface and bottom waters. Redundancy Analysis (RDA) revealed that seasonal variations in community structure were primarily driven by environmental factors such as temperature, dissolved oxygen (DO), and salinity. Co-occurrence network analysis indicated that surface water networks exhibited higher numbers of nodes and edges, as well as greater modularity, suggesting more distinct niche differentiation and higher natural connectivity within the community. These findings provide fundamental data for understanding the response mechanisms of eukaryotic microbial communities to seasonal changes in the mussel cultivation area of Gouqi Island. Full article
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15 pages, 1096 KB  
Article
Myostatin Reduction Within the Myokine–Adipokine Network Predicts Aerobic Adaptation After High-Intensity Interval Training in Combat Athletes
by Eren Bozyilan and Aykut Dundar
Appl. Sci. 2026, 16(7), 3161; https://doi.org/10.3390/app16073161 (registering DOI) - 25 Mar 2026
Abstract
High-intensity interval training (HIIT) is widely used to enhance aerobic performance in combat sports, yet the molecular mechanisms underlying training adaptation remain unclear. This study investigated whether changes in circulating myokine–adipokine profiles are associated with aerobic performance adaptation following sport-specific HIIT in trained [...] Read more.
High-intensity interval training (HIIT) is widely used to enhance aerobic performance in combat sports, yet the molecular mechanisms underlying training adaptation remain unclear. This study investigated whether changes in circulating myokine–adipokine profiles are associated with aerobic performance adaptation following sport-specific HIIT in trained combat athletes. Forty elite male kickboxers were randomly assigned to a HIIT group (n = 20) or a control group (n = 20). The HIIT group performed an eight-week sport-specific HIIT program in addition to regular training, whereas the control group maintained their usual training routines. Aerobic capacity was assessed using maximal oxygen uptake (VO2max). Fasting blood samples were collected before and after the intervention to determine circulating apelin, irisin, brain-derived neurotrophic factor (BDNF), myostatin, fibroblast growth factor-21 (FGF21), and adiponectin concentrations. VO2max increased significantly in the HIIT group compared with the control group (+2.10 ± 1.10 vs. +0.35 ± 0.80 mL·kg−1·min−1, p = 0.001). In addition, apelin, irisin, BDNF, FGF21, and adiponectin increased, whereas myostatin decreased following the intervention. Changes in myostatin were negatively correlated with improvements in VO2max (r = −0.55, p = 0.007), suggesting that reductions in myostatin may serve as a molecular indicator of aerobic adaptation in combat athletes. Full article
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22 pages, 1310 KB  
Article
Effects of Band-Pull Walking Using a Portable Device on Cardiorespiratory and Neuromuscular Responses in Healthy Young Adults
by Ryota Tsuchiya, Hisashi Naito, Shuichi Machida, Keisuke Takamiya and Koji Sugiyama
Sports 2026, 14(4), 130; https://doi.org/10.3390/sports14040130 (registering DOI) - 25 Mar 2026
Abstract
Upper-limb involvement during walking increases metabolic demand compared with normal walking (WK); however, methods such as Nordic walking or hand-held weights require technical skills or may increase mechanical load. This study examined the effects of upper-limb-resisted walking using a novel portable elastic resistance [...] Read more.
Upper-limb involvement during walking increases metabolic demand compared with normal walking (WK); however, methods such as Nordic walking or hand-held weights require technical skills or may increase mechanical load. This study examined the effects of upper-limb-resisted walking using a novel portable elastic resistance device (band-pull walking; BPW) on cardiorespiratory and neuromuscular responses in healthy young adults. Fourteen healthy young adults performed BPW and WK on a treadmill at 60, 80, and 100 m·min−1 in a randomized crossover design. Upper-limb resistance was individually standardized using triceps brachii activity (8% maximum voluntary contraction). Surface electromyography (EMG) of upper- and lower-limb muscles, oxygen uptake, heart rate, and perceived exertion were recorded. BPW significantly increased triceps brachii, biceps brachii, and deltoid muscle activity compared with WK at all or higher speeds (p < 0.05), whereas vastus lateralis and gastrocnemius lateralis activity remained unchanged. Metabolic equivalents and heart rate were higher during BPW across all speeds (p < 0.01), with increases of 8–12%. Upper-limb and whole-body perceived exertion were elevated, whereas lower-limb perceived exertion remained stable. These findings suggest that BPW was associated with increases in upper-limb muscle activation and metabolic demand, whereas no detectable increases were observed in vastus lateralis or gastrocnemius lateralis EMG activity or perceived lower-limb exertion under the present experimental conditions. Full article
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54 pages, 2276 KB  
Review
Targeting NF-κB Signaling with Natural Products: A Promising Therapeutic Strategy for Cardiovascular Diseases
by Rui Liu, Wencong Liu, Ling Dong, Shuang Ma and Baojun Xu
Biomolecules 2026, 16(4), 491; https://doi.org/10.3390/biom16040491 (registering DOI) - 25 Mar 2026
Abstract
Cardiovascular diseases (CVDs) remain the primary cause of human morbidity and mortality in the world. Inflammation, oxidative stress, and vascular remodeling are the key factors that make CVDs worse. The nuclear factor κB (NF-κB) signaling pathway is a major regulator in the progression [...] Read more.
Cardiovascular diseases (CVDs) remain the primary cause of human morbidity and mortality in the world. Inflammation, oxidative stress, and vascular remodeling are the key factors that make CVDs worse. The nuclear factor κB (NF-κB) signaling pathway is a major regulator in the progression of CVDs. NF-κB activates wrongly, induces the secretion of pro-inflammatory cytokines (including TNF-α, IL-6, and IL-1β), and enhances reactive oxygen species (ROS) generation. These accelerate endothelial dysfunction, myocardial damage, and atherosclerotic plaque development. Natural products are structurally diverse, multi-targeted, and low toxicity. They offer a promising way to prevent and treat cardiovascular disease by modulating the NF-κB signaling pathway. This review summarizes the recent studies about using natural products (including flavonoids, terpenoids, alkaloids, polyphenols, and polysaccharides) to treat CVDs through the NF-κB pathway, with a critical analysis of evidence strength according to CVDs indication (atherosclerosis, myocardial ischemia/reperfusion injury, pulmonary arterial hypertension, etc.) and study type (in vitro, in vivo animal, and human clinical research). We detail their molecular mechanisms, such as inhibiting the nuclear translocation of NF-κB p65, downregulating IκB phosphorylation, blocking upstream signaling (e.g., TLR4/MyD88, PI3K/Akt, MAPK), and affecting with other pathways (e.g., Nrf2/HO-1, SIRT1) to reduce inflammation and oxidative stress together. We also detail the effects of these natural products in various CVDs models, including atherosclerosis, hypertension, myocardial ischemia/reperfusion injury, diabetic cardiomyopathy, and pulmonary arterial hypertension, highlighting the characteristics of their treatments. Finally, we discuss the challenges of bringing natural products into the clinic and share some ideas to solve difficulties, with an in-depth critical analysis of the translational bottlenecks (poor bioavailability, unclear structure–activity relationships, incomplete mechanistic elucidation, and lack of large-scale clinical trials) and their underlying causes across different natural product classes. In summary, this review offers new perspectives on developing natural product-based therapies targeting the NF-κB signaling pathway for CVDs. It offers useful references for both preclinical studies and clinical applications. Full article
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25 pages, 5407 KB  
Article
Anti-Tumor Effects of Statins in Pancreatic Ductal Adenocarcinoma Cells
by Veronika Kucháriková, Zuzana Hatoková, Eva Baranovičová, Bibiána Baďurová, Tereza Pavlišová, Lucia Kotúľová, Michal Kalman, Juraj Marcinek, Oľga Chodelková, Slavomíra Nováková, Ján Strnádel, Henrieta Škovierová and Erika Halašová
Int. J. Mol. Sci. 2026, 27(7), 2972; https://doi.org/10.3390/ijms27072972 - 25 Mar 2026
Abstract
Pancreatic ductal adenocarcinoma (PDAC) has limited effective therapeutic strategies. Statins inhibit 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and may affect tumor cell fitness via the mevalonate pathway, mitochondrial function, and redox homeostasis. We systematically compared seven statins in patient-derived PDAC cell lines and related viability [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) has limited effective therapeutic strategies. Statins inhibit 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and may affect tumor cell fitness via the mevalonate pathway, mitochondrial function, and redox homeostasis. We systematically compared seven statins in patient-derived PDAC cell lines and related viability effects to mitochondrial, redox, cell-cycle, apoptotic, and metabolic responses. Statins were tested in three PDAC cell lines (PDAC-1/2/3) using MTT assays (5–20 µM; 24–120 h). Based on MTT responses, mechanistic profiling was performed after 72 h at 20 µM concentration using lipophilic statins, including apoptosis (Annexin V/7-AAD), cell-cycle distribution, mitochondrial membrane potential (Δψm), intracellular ROS, and 1H-NMR quantification of intracellular and extracellular metabolites. Statins reduced viability in a concentration- and time-dependent manner, with lipophilic statins more active than hydrophilic. PDAC-1 was highly sensitive, PDAC-3 intermediate, and PDAC-2 comparatively resistant. PDAC-1 and PDAC-3 showed G0/G1 accumulation, Δψm depolarization, reactive oxygen species (ROS) elevation, and Annexin V–positive apoptosis, whereas PDAC-2 (high basal ROS) showed ROS reduction and limited apoptosis despite Δψm loss. Metabolomics indicated reduced glucose and amino-acid utilization and lactate secretion while preserving line-specific metabolic fingerprints. PDAC cell lines display marked inter-tumoral heterogeneity in statin responses, supporting evaluation of statins as chemosensitizing adjuvants in functionally guided PDAC treatment strategies. Full article
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23 pages, 4014 KB  
Article
CRISPR/Cas9-Mediated Knockout of BnaFAH Enhanced Brassica napus Resistance to Plutella xylostella Under a 2-Day Short-Day Photoperiod
by Tiantian Zhi, Zhou Zhou, Chen Shi, Meiqiong Xie, Gang Chen and Cui Lu
Horticulturae 2026, 12(4), 403; https://doi.org/10.3390/horticulturae12040403 - 24 Mar 2026
Abstract
The diamondback moth (Plutella xylostella) severely threatens global oilseed rape (Brassica napus L.) production. This study demonstrates that CRISPR/Cas9-mediated knockout of two homologous BnaFAH, involved in tyrosine degradation, confers enhanced Brassica napus resistance to Plutella xylostella under a 2-day [...] Read more.
The diamondback moth (Plutella xylostella) severely threatens global oilseed rape (Brassica napus L.) production. This study demonstrates that CRISPR/Cas9-mediated knockout of two homologous BnaFAH, involved in tyrosine degradation, confers enhanced Brassica napus resistance to Plutella xylostella under a 2-day short-day (SD2) photoperiod. Multi-omics analyses revealed that this resistance is associated with a coordinated response: BnaFAH deficiency triggers reactive oxygen species (ROS) accumulation, which is closely associated with activating the jasmonic acid (JA) biosynthetic and signaling pathways. This led to significant upregulation of key JA biosynthetic genes and accumulation of JA, its precursors (OPDA, OPC-4, and OPC-6), and bioactive conjugates (JA-Ile and JA-Phe). Pharmacological analyses support the central role of JA, as exogenous application of methyl jasmonate (MeJA) enhanced insect resistance, whereas the JA biosynthesis inhibitor DIECA suppressed resistance. Scavenging ROS with sodium selenite prevented both JA pathway upregulation and insect resistance, suggesting that ROS may act upstream to activate the JA biosynthetic and signaling pathways. These findings support a previously unrecognized “photoperiod-dependent ROS-JA” defense module, revealing how metabolic perturbation under specific environmental cues can be co-opted to enhance plant immunity, offering new targets for breeding resistant rapeseed varieties. Full article
(This article belongs to the Special Issue Genetics and Molecular Breeding of Brassica Crops)
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