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Cardiometabolic pathologies (CMPs), including cardiovascular diseases, obesity, metabolic syndrome, and type 2 diabetes mellitus (T2DM), are sustained by complex pathophysiological networks in which micronutrient deficiencies, oxidative stress, and chronic inflammation act as interdependent amplifiers. Increasing body of evidence indicates that inadequate levels of key micronutrients—such as vitamins D, E, zinc, selenium, and magnesium—impair the expression and/or activity of endogenous antioxidant enzymes (e.g., superoxide dismutases, glutathione peroxidases, catalase) and disrupt redox-regulatory pathways. This facilitates a shift toward a pro-oxidant intracellular milieu. Mitochondria remain the principal source of intracellular ROS, with complexes I and III of the dysfunctional electron transport system contributing significantly under hyperglycemic or lipotoxic conditions. Additional ROS sources, such as NADPH oxidases (notably NOX2 and NOX4), uncoupled endothelial NO synthase, and monoamine oxidase (MAO), further contribute to the oxidative load. Chronic oxidative stress promotes lipid peroxidation, protein carbonylation, and DNA damage and propagate endothelial, mitochondrial, and metabolic dysfunction. Redox imbalance activates pro-inflammatory transcription factors, particularly NF-κB, and upregulates cytokines such as IL-6, TNF-α, and IL-1β. These cytokines, in turn, further potentiate ROS generation via immune cell recruitment and metabolic reprogramming of macrophages and adipocytes. This forms a self-sustaining loop in which micronutrient deficits impair redox defense, ROS amplify inflammatory signalling, and inflammation further aggravates the redox dyshomeostasis. Restoration of micronutrient sufficiency, re-establishment of redox homeostasis, and targeted anti-inflammatory strategies offer a translational framework for interrupting this pathophysiological vicious circle and alleviating the CMP prognosis. This chapter presents mechanistic insights about the interplay of micronutrient deficiencies, oxidative stress, and inflammation in the setting of CMPs.

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Micronutrient Deficiencies, Oxidative Stress, and Inflammation in Cardiometabolic Pathologies: Three Is a Crowd

  • 章节

  • 发表日期：

    2026年

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  • Adrian Sturza,
  • Adina V. Furdui-Lința,
  • Darius Buriman,
  • Loredana N. Ionică,
  • Rodica Lighezan,
  • Danina M. Muntean

摘要

Cardiometabolic pathologies (CMPs), including cardiovascular diseases, obesity, metabolic syndrome, and type 2 diabetes mellitus (T2DM), are sustained by complex pathophysiological networks in which micronutrient deficiencies, oxidative stress, and chronic inflammation act as interdependent amplifiers. Increasing body of evidence indicates that inadequate levels of key micronutrients—such as vitamins D, E, zinc, selenium, and magnesium—impair the expression and/or activity of endogenous antioxidant enzymes (e.g., superoxide dismutases, glutathione peroxidases, catalase) and disrupt redox-regulatory pathways. This facilitates a shift toward a pro-oxidant intracellular milieu. Mitochondria remain the principal source of intracellular ROS, with complexes I and III of the dysfunctional electron transport system contributing significantly under hyperglycemic or lipotoxic conditions. Additional ROS sources, such as NADPH oxidases (notably NOX2 and NOX4), uncoupled endothelial NO synthase, and monoamine oxidase (MAO), further contribute to the oxidative load. Chronic oxidative stress promotes lipid peroxidation, protein carbonylation, and DNA damage and propagate endothelial, mitochondrial, and metabolic dysfunction. Redox imbalance activates pro-inflammatory transcription factors, particularly NF-κB, and upregulates cytokines such as IL-6, TNF-α, and IL-1β. These cytokines, in turn, further potentiate ROS generation via immune cell recruitment and metabolic reprogramming of macrophages and adipocytes. This forms a self-sustaining loop in which micronutrient deficits impair redox defense, ROS amplify inflammatory signalling, and inflammation further aggravates the redox dyshomeostasis. Restoration of micronutrient sufficiency, re-establishment of redox homeostasis, and targeted anti-inflammatory strategies offer a translational framework for interrupting this pathophysiological vicious circle and alleviating the CMP prognosis. This chapter presents mechanistic insights about the interplay of micronutrient deficiencies, oxidative stress, and inflammation in the setting of CMPs.