Heat stress (HS), induced by global climate warming, is one of the major limiting factors in edible fungi production. HS suppresses mycelial growth and fruiting body formation by causing excessive accumulation of intracellular reactive oxygen species (ROS), disrupting the integrity of cell membranes and cell walls, and impairing cellular metabolism. Increasing evidence suggests that the application of exogenous substances (ESs) effectively mitigates HS in edible fungi. Based on the recent literature, this review categorizes ESs into three groups—core signaling molecules, plant growth regulators, and cytoprotective agents—and summarizes their beneficial effects against HS in edible fungi. The underlying mechanisms of ES-mediated alleviation of heat-induced damage primarily involve four pathways: (1) regulation of antioxidant systems; (2) preservation of cell wall and membrane structural integrity; (3) modulation of defense-related gene expression; and (4) regulation of carbon metabolic flux. Current challenges and corresponding strategies are discussed to provide a reference for elucidating the mechanisms by which ESs alleviate HS and to promote their practical application in edible fungi production.

Heat stress (HS) is a critical bottleneck restricting the commercial cultivation of Pleurotus ostreatus, severely compromising its yield and quality. Glutathione peroxidase (GPX) is a conserved antioxidant enzyme essential for stress adaptation, yet its regulatory mechanism in the fungal heat stress response (HSR) remains unclear. This study characterized a GPX homolog PoGPX in P. ostreatus and elucidated its functions in fungal growth, abiotic stress resistance, and HSR. PoGPX was downregulated during fruiting body development and upregulated under multiple abiotic stresses (especially HS). Silencing PoGPX promoted mycelial growth, biomass accumulation, and hyphal hyperbranching, accompanied by elevated intracellular reactive oxygen species (ROS) levels and compensatory changes in antioxidant enzyme activities. Notably, silencing PoGPX increased cytosolic trehalose content by 0.45-0.62-fold compared with the wild type (WT) strain, and this elevation was reversed by treatment with the ROS scavenger N-acetylcysteine, implying PoGPX modulates trehalose biosynthesis through ROS signaling. Functionally, silencing PoGPX alleviated HS-induced oxidative damage (reduced malondialdehyde content) and suppressed the upregulation of heat shock protein (HSP) genes expression (HSP60, HSP90, HSP104). Critically, inhibiting trehalose biosynthesis restored the HSR phenotypes in PoGPX-silenced strains, indicating trehalose as the key downstream mediator of PoGPX-regulated HSR. These findings uncover that PoGPX regulates HSR in P. ostreatus through trehalose biosynthesis induced by intracellular ROS levels. This study provides novel insights into fungal HSR mechanisms and identifies PoGPX as a promising target for genetic engineering to improve the thermotolerance of P. ostreatus in commercial cultivation. KEY POINTS: • PoGPX acts as a key negative regulator on mycelial growth and hyphal branching in P. ostreatus. • The PoGPX silencing alleviates the heat stress response of P. ostreatus. • PoGPX regulates the heat stress response in P. ostreatus by modulating cytosolic trehalose biosynthesis.