Mitochondrial Dysfunction, Environmental Stressors, and Molecular Mechanisms of Non-Communicable Chronic Diseases

Mitochondrial biology is increasingly recognized as a critical axis in the pathophysiology of non-communicable chronic diseases (NCDs). Mitochondria are central to cellular energetics, metabolic regulation, redox homeostasis, and programmed cell death. Disturbances in mitochondrial integrity or function can undermine cellular equilibrium, raising vulnerability to a spectrum of NCDs such as cardiovascular diseases, neurodegenerative disorders, and various cancers. Recent research underscores the multifaceted influence of mitochondrial dysfunction on disease onset and progression, yet debates persist regarding the relative contributions of genetic, metabolic, and environmental factors. Groundbreaking studies have identified mitochondrial DNA mutations, imbalanced mitochondrial dynamics, and impairments in energy metabolism as pivotal elements, but many mechanistic links remain undefined. Furthermore, the interplay between mitochondria and external environmental factors is an area of expanding interest, emphasizing the need for deeper, integrative investigation.There is increasing recognition that environmental exposures significantly shape mitochondrial health and function, acting as catalysts for cellular distress and disease susceptibility. Exposures to air pollutants, toxicants, heavy metals, ionizing radiation, and lifestyle-associated risks can damage mitochondrial structure, escalate oxidative stress, and distort mitochondrial bioenergetics. These factors may elevate disease risk by compromising mitochondrial DNA integrity, disrupting mitochondrial signaling, and interfering with metabolic communication. Evidence is mounting that mitochondria serve as sensors and effectors within cellular response networks to environmental stressors, but the precise molecular mechanisms that couple these exposures to NCD pathogenesis remain incompletely understood.This Research Topic aims to advance our understanding of the role of mitochondrial dysfunction in non-communicable chronic diseases, with a particular emphasis on the interface between environmental exposures and mitochondrial biology. The objective is to elucidate molecular mechanisms, identify biomarkers of risk or prognosis, and explore intervention strategies that could target mitochondrial pathways for disease modification or prevention.The Scope of this Research Topic encompasses both experimental and clinical studies that investigate the contribution of environmental factors to mitochondrial dysfunction in the context of NCDs. We encourage research spanning basic molecular work, translational investigations, and epidemiological studies. To gather further insights into the connections and underlying pathways, we welcome articles addressing, but not limited to, the following themes:- Molecular consequences of environmental exposures on mitochondrial DNA, dynamics, and bioenergetics- Identification and validation of mitochondrial biomarkers predicting NCD risk or progression- Mechanisms by which mitochondrial dysfunction mediates environmental toxicity and disease development- Therapeutic interventions or lifestyle modifications that mitigate mitochondrial impairment caused by environmental factors- Epidemiological and systems biology approaches linking environmental exposures, mitochondrial changes, and chronic disease outcomesAppendix:Original Research, Review articles, and related article types are welcomed, exploring mechanistic, diagnostic, or therapeutic dimensions related to mitochondrial-environment interactions in chronic diseases. Topic editors: Francesca Gorini, Antonio Rizza, ANDREA BORGHINI, Haotian Wu Source: https://www.frontiersin.org/research-topics/79544/mitochondrial-dysfunction-environmental-stressors-and-molecular-mechanisms-of-non-communicable-chronic-diseases