Heat stress is a major abiotic stress that limits plant biomass production and productivity, especially in tropical and subtropical regions. The photosynthetic machinery is highly sensitive to heat stress, with the photosystem II (PSII) being particularly vulnerable. PSII contains the oxygen-evolving complex (OEC) and is damaged by various stress factors such as drought, salinity, and extreme temperatures. Moderate heat stress does not cause severe PSII damage but inhibits its repair, primarily through de novo protein synthesis, especially of the D1 protein, which is damaged by reactive oxygen species (ROS). This leads to reduced carbon fixation and oxygen evolution, as well as disruption of the linear electron flow. ROS primarily affect the PSII repair system, not directly the PSII reaction center (RC). Heat stress also causes cleavage and aggregation of RC proteins, with unclear mechanisms. Membrane-linked sensors trigger the accumulation of compatible solutes like glycinebetaine and stress proteins that help alleviate ROS-mediated inhibition of repair and are required for acclimation. This review summarizes recent progress in understanding the molecular mechanisms of moderate heat stress on the photosynthetic machinery, especially PSII. Heat stress can be classified into two types: direct damage and inhibition of protein synthesis by ROS. Other stresses like CO2 limitation, drought, cold, or salinity are considered oxidative stresses that inhibit PSII and/or PSI repair. ROS-scavenging mechanisms play an important role in protecting plants against high temperature stress. This review focuses on the effects of moderate high temperature stress in vivo, aiming to dissect and separate the mechanisms of stress injuries, repair processes, and factors affecting the damage-repair cycle. Heat stress can cause damage to various sites, including the CO2 fixation system, photophosphorylation, the electron transport chain, and the OEC. Thylakoid membrane fluidity may act as a sensor for temperature-induced functional changes. A transient elevation in temperature, usually 10-15°C above ambient, is considered heat shock or heat stress. The severity of heat-induced damage depends on the tested system, temperature tolerance, temperature gradient, and mode of heat application. Under in vivo conditions, the heat-stress linked alterations depend on the growth stage of the photosynthetic tissue, with young and old tissues showing different sensitivities. Various parameters of fast Chl fluorescence transients, such as Fv/Fm, Fo, and delayed Chl fluorescence maxima, correlate with heat tolerance. The rise in minimum Chl a fluorescence, Fo level, indicates the critical temperature for PSII inactivation. Early events of heat stress include damage to the Calvin-Benson cycle enzymes, reduced Rubisco activity, and structural changes in Chl-protein complexes and enzyme activity. The macroscopic structure of chloroplasts is also altered by heat exposure, with compromised thylakoid membrane integrity and decreased membrane stacking.Heat stress is a major abiotic stress that limits plant biomass production and productivity, especially in tropical and subtropical regions. The photosynthetic machinery is highly sensitive to heat stress, with the photosystem II (PSII) being particularly vulnerable. PSII contains the oxygen-evolving complex (OEC) and is damaged by various stress factors such as drought, salinity, and extreme temperatures. Moderate heat stress does not cause severe PSII damage but inhibits its repair, primarily through de novo protein synthesis, especially of the D1 protein, which is damaged by reactive oxygen species (ROS). This leads to reduced carbon fixation and oxygen evolution, as well as disruption of the linear electron flow. ROS primarily affect the PSII repair system, not directly the PSII reaction center (RC). Heat stress also causes cleavage and aggregation of RC proteins, with unclear mechanisms. Membrane-linked sensors trigger the accumulation of compatible solutes like glycinebetaine and stress proteins that help alleviate ROS-mediated inhibition of repair and are required for acclimation. This review summarizes recent progress in understanding the molecular mechanisms of moderate heat stress on the photosynthetic machinery, especially PSII. Heat stress can be classified into two types: direct damage and inhibition of protein synthesis by ROS. Other stresses like CO2 limitation, drought, cold, or salinity are considered oxidative stresses that inhibit PSII and/or PSI repair. ROS-scavenging mechanisms play an important role in protecting plants against high temperature stress. This review focuses on the effects of moderate high temperature stress in vivo, aiming to dissect and separate the mechanisms of stress injuries, repair processes, and factors affecting the damage-repair cycle. Heat stress can cause damage to various sites, including the CO2 fixation system, photophosphorylation, the electron transport chain, and the OEC. Thylakoid membrane fluidity may act as a sensor for temperature-induced functional changes. A transient elevation in temperature, usually 10-15°C above ambient, is considered heat shock or heat stress. The severity of heat-induced damage depends on the tested system, temperature tolerance, temperature gradient, and mode of heat application. Under in vivo conditions, the heat-stress linked alterations depend on the growth stage of the photosynthetic tissue, with young and old tissues showing different sensitivities. Various parameters of fast Chl fluorescence transients, such as Fv/Fm, Fo, and delayed Chl fluorescence maxima, correlate with heat tolerance. The rise in minimum Chl a fluorescence, Fo level, indicates the critical temperature for PSII inactivation. Early events of heat stress include damage to the Calvin-Benson cycle enzymes, reduced Rubisco activity, and structural changes in Chl-protein complexes and enzyme activity. The macroscopic structure of chloroplasts is also altered by heat exposure, with compromised thylakoid membrane integrity and decreased membrane stacking.