Adenosine has emerged as a central metabolic signal linking cellular stress to systemic physiological adaptation. Under conditions such as hypoxia, ischemia, inflammation, and tissue injury, extracellular adenosine triphosphate (eATP) released from stressed cells is sequentially metabolized by the ectonucleotidases CD39 and CD73, generating adenosine that accumulates in the extracellular microenvironment. This stress-responsive nucleoside activates four G-protein-coupled receptors (A1, A2A, A2B, and A3), triggering intracellular signaling networks including the cyclic adenosine monophosphate–protein kinase A (cAMP–PKA), mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase–protein kinase B (PI3K–Akt), and hypoxia-inducible factor-1 alpha (HIF-1α) pathways. Through these integrated mechanisms, adenosine orchestrates diverse physiological processes such as vascular regulation, metabolic adaptation, immune modulation, and cellular survival. In the cardiovascular system, adenosine promotes coronary vasodilation and ischemic preconditioning, limiting reperfusion injury. In pulmonary tissues, it mediates acute anti-inflammatory responses but may also drive chronic fibrotic remodeling. Within the central nervous system, adenosine functions as a neuromodulator regulating neuronal excitability, sleep–wake homeostasis, and neuroprotection. In the tumor microenvironment, hypoxia-driven adenosine accumulation suppresses cytotoxic T cell and natural killer activity, facilitating immune evasion and tumor progression. Collectively, adenosine signaling represents a central integrative network that links metabolic stress sensing to coordinated cellular adaptation while simultaneously emerging as a clinically actionable therapeutic target across cardiovascular, inflammatory, neurological, and oncological diseases.

Handgrip strength is a simple and objective measure of muscle function, increasingly associated with physical and psychological health. However, data regarding its link to anxiety and depression in young adults remain limited. The aim of this study was to assess handgrip strength in healthy university students and examine its association with symptoms of anxiety and depression. This cross‐sectional study included 216 undergraduate students (mean age: 20.6 ± 4.7 years). Handgrip strength of each participant was measured using a digital hand dynamometer. Symptoms of anxiety and depression were assessed using the GAD‐7 (Generalized Anxiety Disorder‐7) and the PHQ‐9 (Patient Health Questionnaire‐9), respectively. Pearson correlations and independent sample t ‐tests were used for statistical analysis. Handgrip strength showed a small but statistically significant negative correlation with PHQ‐9 (left hand: r = −0.148, p = 0.030) and GAD‐7 (left hand: r = −0.185, p = 0.006) scores. These associations were stronger in female participants. Anxiety and depression scores were strongly positively correlated ( r = 0.705, p < 0.001). The results of this study indicate lower handgrip strength was associated with higher anxiety and depression symptoms in healthy university students, especially in female students. However, further longitudinal studies are needed to establish causality.