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.

Low-temperature storage is used to extend the shelf life of fruits, but prolonged storage at temperatures below tolerable levels may cause postharvest chilling injury (PCI) in sensitive commodities. This review aims to highlight adenosine triphosphate (ATP) activation and the interplay of extracellular ATP (eATP) and intracellular ATP (iATP) in fruits and to find out its significance in mitigating PCI. Various pathways, such as the Embden–Meyerhof–Parnas pathway, the tricarboxylic acid cycle, the pentose phosphate pathway, the γ-aminobutyric acid shunt pathway, and the cytochrome pathway, are studied critically to elucidate their role in continuous ATP supply and maintaining the membrane fluidity and integrity. This review summarizes the treatments helpful in modulating energy metabolism in fruit. Additionally, this work provides insights into the energy status in attenuating chilling tolerance. Moreover, it states the potential of nicotinamide adenine dinucleotide in mitigating PCI. Furthermore, it discusses the role of eATP and its receptor DORN1 in mitigating chilling stress.

Peach being a climacteric fruit has a limited shelf life. Cold storage of peaches is an essential measure to maintain their quality. However, prolonged exposure to cold temperatures causes chilling injury in peaches, resulting in significant economic losses. Approximately, 40 of the produced commodity is lost in postharvest handling in which chilling injury contributes to about 25. Melatonin can be a green solution and plays a key role in protecting peaches from chilling injury. Therefore, this experiment aimed to determine the effect of melatonin on the Silver King peaches by dipping them in 100μM melatonin for 2hours followed by storing them at chilling temperatures of 2±1°C and 9095 relative humidity for 21d. The results showed that while control fruit experienced chilling injury and poor fruit quality, increased respiration rate, and enhanced senescence, 100μM melatonin treatment was successful in preserving the fruit quality at chilling temperatures and was associated with the delayed respiration rate and lower malondialdehyde levels, along with the preservation of certain physicochemical parameters, namely, total soluble solids, pH, fruit firmness, and titratable acidity. Moreover, a 1.5 times higher proline concentration was observed in melatonin-treated peaches when compared to that of nontreated peaches. This rise was linked to the enhanced activity of Δ¹-pyrroline-5-carboxylate synthetase and ornithine-δ-aminotransferase along with a decrease in the activity of proline dehydrogenase during 21d of storage.