High temperatures seriously threaten the global yield of maize. The objectives of the present study were to explore the key candidate gene involved in heat shock responses in maize and its potential biological function to heat stress. Here, we identified a Class C heat shock factor, ZmHSF21, from maize leaves and used molecular biological and plant physiological assays to investigate its roles in transgenic Arabidopsis. ZmHSF21 encodes a putative protein of 388 amino acids. We showed that ZmHSF21 was expressed in most tissues of maize with relatively high expression in leaves and silks but rather low in roots and stalks, and its expression level in leaves was significantly up-regulated by heat treatment. We also showed that overexpression of ZmHSF21 in Arabidopsis significantly improved the seed germination frequency and plant survival rate when exposed to heat stress. We demonstrated that, compared with wild-type plants, the activities of peroxidase, superoxide dismutase, and catalase increased while the reactive oxygen species accumulation decreased in ZmHSF21 overexpressors under heat stress conditions. We further demonstrated that ZmHSF21 promoted the transcriptional level of AtAPX2, AtGolS1, and several AtHSPs. Collectively, the first-class C HSF in maize (ZmHSF21) is cloned in this study, and the combined results suggest that ZmHSF21 is a positive regulator of heat shock response and can be applied to develop maize high-temperature-tolerant varieties for more yield.

Reactive oxygen species (ROS) exert dual biological functions in plants. Though they form toxic byproducts of aerobic metabolism, ROS also serve as indispensable secondary messengers that orchestrate stress acclimation programs. For decades, plant physiologists operated under a pervasive assumption that constitutive and non-compartmentalized upregulation of antioxidant capacity would universally enhance abiotic stress tolerance. This long-standing dogma has now been thoroughly overturned. A growing body of evidence shows that sustained, global high antioxidant activity often impairs adaptation rather than helping it. In this review, we replace the simplistic “more antioxidants equal better tolerance” framework with a dynamic model of cellular redox homeostasis. We dissect three interconnected mechanisms though which unrestrained ROS scavenging generates deleterious phenotypic outcomes. First, indiscriminate clearance blunts transient ROS pulses and propagating ROS waves, the core signaling events acquired to trigger systemic acquired acclimation (SAA). Second, continuous antioxidant biosynthesis drains finite carbon skeletons, NADPH, and ATP pools, exacerbating evolutionary growth-defense resource trade-offs. Third, non-specific bulk ROS scavenging erases compartment-specific organellar retrograde signals, which rely on tightly controlled spatial and temporal ROS fluctuations. We concurrently define physiological boundary conditions where robust antioxidant activity remains vital for plant survival under extreme stress. Rather than advocating for the complete suppression of ROS detoxification, our analysis advocates context-dependent fine-tuning of redox signaling networks. We also summarize emerging precision redox monitoring and genetic engineering tools, and outline translational breeding pipelines to develop climate-resilient crops that balance stress survival and yield stability. This work delivers novel conceptual perspectives to advance fundamental plant redox biology.