Rising atmospheric CO2 is a key driver of climate change, intensifying drastic changes
in meteorological parameters. Plants can sense and respond to changes in environmental
parameters including atmospheric CO2 and temperatures. High temperatures beyond the
physiological threshold can significantly affect plant growth and development and
thus attenuate crop productivity. However, elevated atmospheric CO2 can mitigate the
deleterious effects of heat stress on plants. Despite a large body of literature supporting
the positive impact of elevated CO2 on thermotolerance, the underlying biological
mechanisms and precise molecular pathways that lead to enhanced tolerance to heat
stress remain largely unclear. Under heat stress, elevated CO2-induced expression
of respiratory burst oxidase homologs (RBOHs) and reactive oxygen species (ROS) signaling
play a critical role in stomatal movement, which optimizes gas exchange to enhance
photosynthesis and water use efficiency. Notably, elevated CO2 also fortifies antioxidant
defense and redox homeostasis to alleviate heat-induced oxidative damage. Both hormone-dependent
and independent pathways have been shown to mediate high CO2-induced thermotolerance.
The activation of heat-shock factors and subsequent expression of heat-shock proteins
are thought to be the essential mechanism downstream of hormone and ROS signaling.
Here we review the role of phytohormones in plant response to high atmospheric CO2
and temperatures. We also discuss the potential mechanisms of elevated CO2-induced
thermotolerance by focusing on several key phytohormones such as ethylene. Finally,
we address some limitations of our current understanding and the need for further
research to unveil the yet-unknown crosstalk between plant hormones in mediating high
CO2-induced thermotolerance in plants.