Soil salinity is the major limiting factor restricting plant growth and development. Little is known about the comparative and combined effects of gibberellic acid (GA₃) seed priming and foliar application on maize under salt stress. The current study determined the impact of different application methods of GA₃ on morpho-physiological, biochemical and molecular responses of maize seedlings under three salinity stress treatments (no salinity, moderate salinity-6 dS m⁻¹, and severe salinity-12 dS m⁻¹). The GA₃ treatments consisted of control, hydro-priming (HP), water foliar spray (WFS), HP + WFS, seed priming with GA₃ (GA₃P, 100 mg L⁻¹), foliar spray with GA₃ (GA₃FS, 100ppm) and GA₃P + GA₃FS. Salt stress particularly at 12 dS m⁻¹ reduced the length of shoots and roots, fresh and dry weights, chlorophyll, and carotenoid contents, K⁺ ion accumulation and activities of antioxidant enzymes, while enhanced the oxidative damage and accumulation of the Na⁺ ion in maize plants. Nevertheless, the application of GA₃ improved maize growth, reduced oxidative stress, and increased the antioxidant enzymes activities, antioxidant genes expression, and K⁺ ion concentration under salt stress. Compared with control, the GA₃P + GA₃FS recorded the highest increase in roots and shoots length (19–37%), roots fresh and dry weights (31–43%), shoots fresh and dry weights (31–47%), chlorophyll content (21–70%), antioxidant enzymes activities (73.03–150.74%), total soluble protein (13.05%), K⁺ concentration (13–23%) and antioxidants genes expression levels under different salinity levels. This treatment also reduced the H₂O₂ content, and Na⁺ ion concentration. These results indicated that GA₃P + GA₃FS could be used as an effective tool for improving the maize growth and development, and reducing the oxidative stress in salt-contaminated soils.

The recent acceleration of commercial, private, and multi-national spaceflight has created an unprecedented level of activity in low Earth orbit (LEO), concomitant with the highest-ever number of crewed missions entering space and preparations for exploration-class (>1 year) missions. Such rapid advancement into space from many new companies, countries, and space-related entities has enabled a“Second Space Age.” This new era is also poised to leverage, for the first time, modern tools and methods of molecular biology and precision medicine, thus enabling precision aerospace medicine for the crews. The applications of these biomedical technologies and algorithms are diverse, encompassing multi-omic, single-cell, and spatial biology tools to investigate human and microbial responses to spaceflight. Additionally, they extend to the development of new imaging techniques, real-time cognitive assessments, physiological monitoring, and personalized risk profiles tailored for astronauts. Furthermore, these technologies enable advancements in pharmacogenomics (PGx), as well as the identification of novel spaceflight biomarkers and the development of corresponding countermeasures. In this review, we highlight some of the recent biomedical research from the National Aeronautics and Space Administration (NASA), Japan Aerospace Exploration Agency (JAXA), European Space Agency (ESA), and other space agencies, and also detail the commercial spaceflight sector’s (e.g. SpaceX, Blue Origin, Axiom, Sierra Space) entrance into aerospace medicine and space biology, the first aerospace medicine biobank, and the myriad upcoming missions that will utilize these tools to ensure a permanent human presence beyond LEO, venturing out to other planets and moons.

Gravity is the only component of Earth environment that remained constant throughout the entire process of biological evolution. However, it is still unclear how gravity affects plant growth and development. In this study, an in vitro cell culture of Arabidopsis thaliana was exposed to different altered gravity conditions, namely simulated reduced gravity (simulated microgravity, simulated Mars gravity) and hypergravity (2g), to study changes in cell proliferation, cell growth, and epigenetics. The effects after 3, 14, and 24-hours of exposure were evaluated. The most relevant alterations were found in the 24-hour treatment, being more significant for simulated reduced gravity than hypergravity. Cell proliferation and growth were uncoupled under simulated reduced gravity, similarly, as found in meristematic cells from seedlings grown in real or simulated microgravity. The distribution of cell cycle phases was changed, as well as the levels and gene transcription of the tested cell cycle regulators. Ribosome biogenesis was decreased, according to levels and gene transcription of nucleolar proteins and the number of inactive nucleoli. Furthermore, we found alterations in the epigenetic modifications of chromatin. These results show that altered gravity effects include a serious disturbance of cell proliferation and growth, which are cellular functions essential for normal plant development.

Mechanical unloading leads to profound musculoskeletal degeneration, muscle wasting, and weakness. Understanding the specific signaling pathways involved is essential for uncovering effective interventions. This review provides new perspectives on mechanotransduction pathways, focusing on the critical roles of focal adhesions (FAs) and oxidative stress in skeletal muscle atrophy under mechanical unloading. As pivotal mechanosensors, FAs integrate mechanical and biochemical signals to sustain muscle structural integrity. When disrupted, these complexes impair force transmission, activating proteolytic pathways (e.g., ubiquitin–proteasome system) that accelerate atrophy. Oxidative stress, driven by mitochondrial dysfunction and NADPH oxidase-2 (NOX2) hyperactivation, exacerbates muscle degeneration through excessive reactive oxygen species (ROS) production, impaired repair mechanisms, and dysregulated redox signaling. The interplay between FA dysfunction and oxidative stress underscores the complexity of muscle atrophy pathogenesis: FA destabilization heightens oxidative damage, while ROS overproduction further disrupts FA integrity, creating a self-amplifying vicious cycle. Therapeutic strategies, such as NOX2 inhibitors, mitochondrial-targeted antioxidants, and FAK-activating compounds, promise to mitigate muscle atrophy by preserving mechanotransduction signaling and restoring redox balance. By elucidating these pathways, this review advances the understanding of muscle degeneration during unloading and identifies promising synergistic therapeutic targets, emphasizing the need for combinatorial approaches to disrupt the FA-ROS feedback loop.