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This paper tells the story of how hormesis became recognized as a fundamental concept in biology, affecting toxicology, microbiology, medicine, public health, agriculture, and all areas related to enhancing biological performance. This paper assesses how hormesis enhances resilience to normal aging and protects against a broad spectrum of neurodegenerative, cardiovascular, and other diseases, as well as trauma and other threats to health and well-being. This paper also explains the application of hormesis to several neurodegenerative diseases such as Parkinson’s and Huntington’s disease, macrophage polarization and its systematic adaptive protections, and the role of hormesis in enhancing stem cell functioning and medical applications.

Hormesis, which describes the stimulatory effect of low doses of toxic substances on growth, is a well-known phenomenon in the plant and animal kingdoms. However, the mechanisms that are involved in this phenomenon are still poorly understood. We performed preliminary studies on corn coleoptile sections, which showed a positive correlation between the stimulation of growth by Cd or Pb and an increase in the auxin and H2O2 content in the coleoptile sections. Subsequently, we grew corn seedlings in hydroponic culture and tested a wide range of Cd or Pb concentrations in order to determine hormetic growth stimulation. In these seedlings the gas exchange and the chlorophyll a fluorescence, as well as the content of chlorophyll, flavonol, auxin and hydrogen peroxide, were measured. We found that during the hormetic stimulation of growth, the response of the photosynthetic apparatus to Cd and Pb differed significantly. While the application of Cd mostly caused a decrease in various photosynthetic parameters, the application of Pb stimulated some of them. Nevertheless, we discovered that the common features of the hormetic stimulation of shoot growth by heavy metals are an increase in the auxin and flavonol content and the maintenance of hydrogen peroxide at the same level as the control plants.

Employing a developmental psychopathology framework, we tested the utility of the hormesis model in examining the strengthening of children and youth through limited levels of adversity in relation to internalizing and externalizing outcomes within a brain-by-development context. Analyzing data from the Adolescent Brain and Cognitive Development study ( = 11,878), we formed latent factors of threat, deprivation, and unpredictability. We examined linear and nonlinear associations between adversity dimensions and youth psychopathology symptoms and how change of resting-state functional connectivity (rsFC) in the default mode network (DMN) from Time 1 to Time 5 moderates these associations. A cubic association was found between threat and youth internalizing problems; low-to-moderate family conflict levels reduced these problems. Deprivation also displayed a cubic relation with youth externalizing problems, with moderate deprivation levels associated with fewer problems. Unpredictability linearly increased both problem types. Change in DMN rsFC significantly moderated the cubic link between threat levels and internalizing problems, with declining DMN rsFC levels from Time 1 to Time 5 facilitating hormesis. Hormetic effects peaked earlier, emphasizing the importance of sensitive periods and developmental timing of outcomes related to earlier experiences. Strengthening through limited environmental adversity is crucial for developing human resilience. Understanding this process requires considering both linear and nonlinear adversity-psychopathology associations. Testing individual differences by brain and developmental context will inform preventive intervention programming.

Protein synthesis, or mRNA translation, is one of the most energy-consuming functions in cells. Translation of mRNA into proteins is thus highly regulated by and integrated with upstream and downstream signaling pathways, dependent on various transacting proteins and cis-acting elements within the substrate mRNAs. Under conditions of stress, such as exposure to ionizing radiation, regulatory mechanisms reprogram protein synthesis to translate mRNAs encoding proteins that ensure proper cellular responses. Interestingly, beneficial responses to low-dose radiation exposure, known as radiation hormesis, have been described in several models, but the molecular mechanisms behind this phenomenon are largely unknown. In this review, we explore how differences in cellular responses to high- vs. low-dose ionizing radiation are realized through the modulation of molecular pathways with a particular emphasis on the regulation of mRNA translation control.

Both inhibitory and stimulatory (known as hormesis) effects of the sublethal flupyradifurone, a butenolide insecticide, on Myzus persicae Sulzer (Hemiptera: Aphididae) were investigated for incorporating it into integrated pest management (IPM). A leaf-dip bioassay showed that flupyradifurone was very toxic against adult M. persicae with a 48 h LC50 of 8.491 mg/L. Using the age-stage two-sex life table approach, we assessed the effects of LC25 of flupyradifurone on adult M. persicae and its progeny (F1 and F2). On the one hand, aphids exposed to flupyradifurone had significantly negative effects on the life history traits acrossing the generations, such as reduced the adult longevity and fecundity of F0, shortened the duration of third instar and fourth instar nymphs, preadult period and the pre-reproductive period of F1, and decreased the reproductive days and adult longevity of F2. On the other hand, stimulatory effects on the duration of pre-adult, adult reproductive days, and reproduction of F1 were observed in the flupyradifurone-treated aphids. Consistently with the stimulation on individual traits, a higher net reproductive rate (R0) of F1 and a shorter mean generation time (T) of F2 were observed in the flupyradifurone-treated aphids, although the other population parameters including the intrinsic rate of increase (r), finite rate of increase (λ) and T of F1 and R0, r and λ of F2 were not significantly affected. These results revealed that adult M. persicae exposed to sublethal concentration of flupyradifurone can induce hormetic effects on F1, and also cause negative effects on F2. Our results would be useful for assessing the overall effects of flupyradifurone on M. persicae and the hormetic effects should take into consideration when use flupyradifurone for control M. persicae.

It is widely acknowledged that aging, mitochondrial dysfunction, and cellular phenotypic abnormalities are intricately associated with the degeneration of bone and cartilage. Consequently, gaining a comprehensive understanding of the regulatory patterns governing mitochondrial function and its underlying mechanisms holds promise for mitigating the progression of osteoarthritis, intervertebral disc degeneration, and osteoporosis. Mitochondrial hormesis, referred to as mitohormesis, represents a cellular adaptive stress response mechanism wherein mitochondria restore homeostasis and augment resistance capabilities against stimuli by generating reactive oxygen species (ROS), orchestrating unfolded protein reactions (UPRmt), inducing mitochondrial-derived peptides (MDP), instigating mitochondrial dynamic changes, and activating mitophagy, all prompted by low doses of stressors. The varying nature, intensity, and duration of stimulus sources elicit divergent degrees of mitochondrial stress responses, subsequently activating one or more signaling pathways to initiate mitohormesis. This review focuses specifically on the effector molecules and regulatory networks associated with mitohormesis, while also scrutinizing extant mechanisms of mitochondrial dysfunction contributing to bone and cartilage degeneration through oxidative stress damage. Additionally, it underscores the potential of mechanical stimulation, intermittent dietary restrictions, hypoxic preconditioning, and low-dose toxic compounds to trigger mitohormesis, thereby alleviating bone and cartilage degeneration.

Oxidation–reduction (redox) reactions are central to the existence of life. Reactive species of oxygen, nitrogen and sulfur mediate redox control of a wide range of essential cellular processes. Yet, excessive levels of oxidants are associated with ageing and many diseases, including cardiological and neurodegenerative diseases, and cancer. Hence, maintaining the fine-tuned steady-state balance of reactive species production and removal is essential. Here, we discuss new insights into the dynamic maintenance of redox homeostasis (that is, redox homeodynamics) and the principles underlying biological redox organization, termed the ‘redox code’. We survey how redox changes result in stress responses by hormesis mechanisms, and how the lifelong cumulative exposure to environmental agents, termed the ‘exposome’, is communicated to cells through redox signals. Better understanding of the molecular and cellular basis of redox biology will guide novel redox medicine approaches aimed at preventing and treating diseases associated with disturbed redox regulation.Oxidation–reduction (redox) reactions involving reactive oxygen, nitrogen and sulfur species are vital for life, but excessive oxidant levels contribute to ageing and diseases. This Review explores cellular dynamics of redox homeostasis, such as responses to oxidative and reductive stresses and intracellular and intercellular redox communication pathways.

•Poor dietary choices and physical inactivity are the leading causes of death from stroke, heart disease, and cancer worldwide.•Chronic overnutrition triggers can lead to diabetes, atherosclerosis, and hypertension through mechanisms triggered by chronic glycemic and lipid overload.•“Cellular exercise” is a concept where low levels of cellular stress, induced by chronic calorie restriction or physical exercise, can lead to molecular adaptations on the cellular level that can protect the body from cancer and cardiovascular disease.•An increase in reactive oxygen species induced by caloric restriction and physical exercise can activate nuclear factor erythroid and phase II improvements in redox equilibrium that can result in a more adaptive capable cell.•Insulin-like growth factor-1 has a dual effect wherein calorie restriction downregulates insulin-like growth factor-1 inhibiting pathways of carcinogenic proliferation and metastasis and physical exercise can upregulate insulin-like growth factor-1 to promote mitochondrial biogenesis and protein synthesis thereby strengthening healthy muscle against hypoxic ischemic damage and muscular regenerative properties.•Transcription of Nrf2 is also upregulated to attenuate inflammation induced by nuclear factor-κB, AMPK upregulates genes through PGC-1α to prevent sarcopenia and induce lipolysis.•This molecular melody is the complex composition that explains the cellular adaption that occurs to strengthen the body from cognitive dysfunction, cardiometabolic failure and carcinogenic implantation and metastasis via mechanisms of redox equilibrium, oxidative protection, attenuation of inflammation, and attenuation of carcinogenic proliferation and growth. Overnutrition is a poor dietary habit that has been correlated with increased health risks, especially in the developed world. This leads to an imbalance between energy storage and energy breakdown. Many biochemical processes involving hormones are involved in conveying the excess of energy into pathologic states, mainly atherosclerosis, hypertension, cardiovascular diseases, and diabetes. Diverse modalities of regular exercise have been shown to be beneficial, to varying extents, in overcoming the overnutrition comorbidities. Cellular exercises and hormesis are triggered by dietary protocols that could underlie the cellular mechanisms involved in modulating the deleterious effects of overnutrition through activation of specific cellular signal pathways. Of interest are the oxidative stress signaling, nuclear factor erythroid-2, insulin-like growth factor-1, AMP-activated protein kinase as well as sirtuins and nuclear factor-κB. Therefore, the value of intermittent fasting diets as well as different diet regimens inducing hormesis are evaluated in terms of their beneficial effects on health and longevity. In parallel, important effects of diets on the immune system are explored as essential components that can undermine the overall health outcome. Additionally, the subtle but relevant relation between diet and sleep is investigated for its impact on the cardiovascular system and quality of life. The aim of this review is to focus on how calorie restriction triggers multiple molecular pathways that ultimately lead to hormetic effects resulting in cell longevity and resistance to cardiovascular disease, stroke, and cancer.

As one of the most toxic environmental pollutants, cadmium (Cd) has lastingly been considered to have negative influences on plant growth and productivity. Recently, increasing studies have shown that low level of Cd exposure could induce hormetic effect which benefits to plants. However, the underlying mechanisms of Cd-triggered hormesis are poorly understood. In this study, we found that Cd stress treatment showed a hormetic effect on peppermint and Cd treatment with 1.6 mg L -1 concertation manifested best stimulative effects. To explore the hormesis mechanisms of Cd treatment, comparative transcriptome analysis of peppermint young plants under low (1.6 mg L -1 ) and high (6.5 mg L -1 ) level of Cd exposure at 0 h, 24 h and 72 h were conducted. Twelve of differentially expressed genes (DEGs) were selected for qRT-PCR validation, and the expression results confirmed the credibility of transcriptome data. KEGG analysis of DEGs showed that the phenylpropanoid biosynthesis and photosynthesis were important under both low and high level of Cd treatments. Interestingly, GO and KEGG analysis of 99 DEGs specifically induced by low level of Cd treatment at 72 h indicated that these DEGs were mainly involved in the pathway of phenylpropanoid biosynthesis and their functions were associated with antioxidant activity. The expression pattern of those genes in the phenylpropanoid biosynthesis pathway and encoding antioxidant enzymes during 72 h of Cd exposure showed that low level of Cd treatment induced a continuation in the upward trend but high level of Cd treatment caused an inverted V-shape. The changes of physiological parameters during Cd exposure were highly consistent with gene expression pattern. These results strongly demonstrate that low level of Cd exposure constantly enhanced antioxidant activity of peppermint to avoid oxidative damages caused by Cd ion, while high level of Cd stress just induced a temporary increase in antioxidant activity which was insufficient to cope with lasting Cd toxicity. Overall, the results presented in this study shed a light on the underlying mechanisms of the Cd-mediated hormesis in plant. Moreover, our study provided a safe method for the efficient utilization of mild Cd-contaminated soil as peppermint is an important cash plant.

Heat hormesis describes the beneficial adaptations resulting from transient exposure to mild heat stress, which enhances stress resilience and promotes healthy aging. While heat hormesis is widely observed, much remains to be learned about its molecular basis. This study bridges a critical knowledge gap through a comprehensive multiomic analysis, providing key insights into the transcriptomic and chromatin accessibility landscapes throughout a heat hormesis regimen in Caenorhabditis elegans . We uncover highly dynamic, dose-dependent molecular responses to heat stress and reveal that while most initial molecular changes induced by mild stress revert to baseline, key differences emerge in response to subsequent heat shock challenge that likely contribute to physiological benefits. We further demonstrate that heat hormesis extends life span specifically in wild-type animals, but not in germline-less mutants, likely due to transient disruption of germline activities during mild heat exposure, which appears sufficient to trigger pro-longevity mechanisms. This finding points to tissue-specific responses in mediating the physiological outcomes of heat hormesis. Importantly, we identify several highly conserved regulators of heat hormesis that likely orchestrate gene expression to enhance stress resilience. Among these regulators, some (MARS-1/MARS1, SNPC-4/SNAPc, FOS-1/c-Fos) are broadly required for heat-hormesis-induced benefits, whereas others (ELT-2/GATA4, DPY-27/SMC4) are uniquely important in specific genetic backgrounds. This study advances our understanding of stress resilience mechanisms, points to multiple new avenues for future investigations, and provides a molecular framework for promoting healthy aging through strategic mid-life stress management.