The adaptation of plants to biotic and abiotic stress depends on their abilities to sense their surroundings and to generate and transmit corresponding signals to different parts of their body that can evoke changes necessary for optimizing growth and defense. Light has been shown to be one of the key environmental factors that modulate the physiology of both plants and animals via the diverse photoreceptors found in them. Both plants and animals contain a large repertoire of intra- and intercellular signals molecules that include organic and inorganic. One such molecule is a neurotransmitter, γ-aminobutyric acid (GABA), a non-protein amino acid, that rapidly accumulates in plant tissues in response to biotic and abiotic stress and regulates plant growth. Lots of research has been done on GABA in plants for slightly more than half a century now: Its discovery in plant tissues was immediately followed by physiological and biochemical studies. Thereafter molecular-genetics era of cloning the genes encoding the GABA shunt enzymes and transporters, and recombinant expression and purification of the enzymes in vitro to elucidate their regulatory properties and substrate specificity was established. Recently the discovery of the first bona fide GABA target proteins in plants, the ALMTs suggest that GABA indeed could be one of the signaling molecules in plants. All this research did not address in detail the relationship between light and GABA. To better understand the role of GABA in relation to light we set up six light conditions to investigate the changes in the hypocotyl and root growth in Arabidopsis thaliana under different light conditions, including total light, total dark, light blocker, gradient light, shoot dark, shoot dark with blocker. We treated the seedlings with 3-MPA, a GABA inhibitor, using different concentrations grown under different light conditions between 24 to 96 h. Our results show that both the root and hypocotyl are modulated by GABA when grown under different light conditions. These results clearly suggest a link in the signaling pathway of GABA with photoreceptor signaling pathways.

Background/Objectives: Pulmonary hypertension associated with chronic lung disease remains difficult to diagnose, phenotype, and manage because vascular remodeling, parenchymal lung injury, hypoxemia, inflammation, fibrosis, and right ventricular dysfunction often coexist. Natriuretic peptides are widely used as cardiopulmonary biomarkers, but the receptor-level role of natriuretic peptide receptor-C, encoded by NPR3, remains incompletely defined. This scoping review mapped original empirical evidence on NPR-C/NPR3 and related C-type natriuretic peptide biology in pulmonary hypertension, chronic lung disease, pulmonary vascular remodeling, and right ventricular adaptation. Methods: This scoping review was conducted and reported in accordance with PRISMA-ScR, with applicable PRISMA 2020 reporting elements addressed where relevant to a scoping review. Searches of PubMed/MEDLINE and APA PsycINFO identified 72 records. After removal of 2 duplicates, 70 records underwent title and abstract screening. Forty-two records were excluded at this stage, and 28 reports were sought for full-text retrieval. All reports were retrieved and assessed for eligibility. Eleven reports were excluded at full-text review, leaving 17 original studies for inclusion in the evidence map. Reviews, meta-analyses, editorials, commentaries, protocols, and non-original reports were excluded from the synthesis. Results: The included studies comprised clinical biomarker studies, transcriptomic and receptor-expression analyses, experimental pulmonary hypertension models, chronic lung injury or fibrosis models, and pulmonary vascular cellular studies. Human evidence directly addressing chronic lung disease-associated pulmonary hypertension was limited and largely biomarker-centered, with CNP or NT-proCNP signals suggesting potential relevance to pulmonary vascular stress but without definitive NPR-C/NPR3 validation. Experimental studies supported biologic plausibility, linking CNP/NPR-C-related pathways to endothelial function, pulmonary vascular remodeling, smooth muscle and fibroblast behavior, hypoxic signaling, fibrosis, and right ventricular remodeling. However, findings varied across models, and receptor-specific attribution to NPR-C/NPR3 was often incomplete. Conclusions: Current evidence suggests that NPR-C/NPR3 is a biologically plausible but not yet clinically validated pathway in pulmonary hypertension associated with chronic lung disease. The strongest gap is the absence of prospective human studies integrating invasive hemodynamics, lung disease phenotyping, CNP/NT-proCNP profiling, NPR3 expression or genetic assessment, receptor-level biology, and right ventricular outcomes. Future studies should determine whether NPR-C/NPR3 can improve phenotyping, risk stratification, or therapeutic targeting in chronic lung disease-associated pulmonary hypertension.