Molecular Biochemistry and Physiology of Postharvest Chilling Injury in Fruits: Mechanisms and Mitigation

Postharvest chilling injury (PCI) is a significant limitation in the storage of temperature-sensitive fruits, leading to quality deterioration and reduced marketability. However, low temperatures delay senescence—consistent with the Q10 principle, where metabolic reaction rates change 2–3-fold per 10 °C—and chilling-sensitive fruits experience membrane destabilization, oxidative imbalances, and structural degradation under cold stress. Physiological assessments consistently report elevated electrolyte leakage, increased malondialdehyde accumulation, and reduced membrane fluidity, coupled with disruptions in respiration and cellular energy metabolism. Biochemically, PCI is characterized by enhanced ROS production and a 20–50% decline in key antioxidant enzymes, along with disturbances in calcium signaling and hormone regulation. At the molecular level, chilling-responsive transcription factors such as CBF, CAM, HSF, and WRKY show strong induction, while lipid remodeling and epigenetic modifications further shape cold adaptation responses. Advances in multi-omics, including transcriptomics, proteomics, metabolomics, lipidomics, and volatilomics, have revealed chilling-associated metabolic shifts and regulatory cascades, enabling the identification of potential biomarkers of tolerance. Emerging mitigation strategies, including physical and chemical treatments, as well as CRISPR-based interventions, have shown a 30–60% reduction in PCI in controlled studies. This review synthesizes recent progress in physiology, molecular biochemistry, and postharvest technology to support future research and practical PCI management.