Résumé
À partir des années 1960, l’idée que la vaste majorité des maladies humaines ne sont ni le résultat d’une exposition environnementale isolée ni celui de la mutation d’un gène unique s’est imposée : le plus souvent, les effets des facteurs de risque génétiques et environnementaux se conjuguent. Quelques années plus tard, des expériences ont montré que des modifications cellulaires acquises peuvent entraîner des changements persistants de l’expression des gènes et peuvent être transmises d’une génération à l’autre : on aborde le champ de l’épigénétique. Le présent article tend à expliquer ces mécanismes, et à citer des exemples de chacun d’eux. Les polluants de l’environnement à risque incluent par exemple les polluants de l’air, les métaux lourds (plomb et mercure), les retardateurs de flamme et certains pesticides. Les effets critiques examinés sont la croissance foetale et la prématurité, le développement neurologique et cognitif, la santé respiratoire et immunologique, la croissance de l’enfant et l’obésité. Parmi les anomalies congénitales qui résultent d’une interaction gènes–environnement, les défauts de fermeture du tube neural, les fentes faciales et les cardiopathies sont fréquemment mentionnés. L’apport de la notion récente d’épigénétique est le fait que l’alimentation, l’air respiré et même les émotions pourraient influencer non seulement l’expression des gènes d’un individu, mais celle de ses enfants et de ses petits-enfants. Ainsi, la dénutrition, la suralimentation ou encore le stress sont susceptibles d’induire aux générations suivantes des pathologies aussi variées qu’obésité, diabète, allergies ou maladies cardiovasculaires. Les résultats des études citées pourraient avoir des conséquences importantes pour la connaissance des facteurs de risque, la prévention ou même le traitement de nombreuses maladies.
Abstract
Beginning in the 1960s, the idea that the vast majority of human diseases are neither the result of isolated environmental exposures nor that of the mutation of a single gene was imposed: genetic and environmental risks often are combined. A few years later, experiments have shown that acquired cell changes can lead to persistent changes in gene expression and can be transmitted from one generation to another: the field of epigenetics was born. This article attempts to explain these mechanisms and to give examples. At risk pollutants in the environment include, for example, air pollutants, heavy metals (lead and mercury), flame retardants, and certain pesticides. The critical effects examined are fetal growth and prematurity, neurological and cognitive development, respiratory and immunological health, child growth, and obesity. Among the congenital abnormalities, those that are best known as a result of a gene–environment interaction are neural tube defects, facial clefts, and heart diseases. The recent concept of epigenetics and transgenerational heredity indicates that diet, breathed air, and even emotions might influence not only the expression of an individual’s genes but that of his children and grandchildren. Thus, undernutrition, overeating, or stress is likely to induce in the next generations pathologies as varied as obesity, diabetes, allergies, or cardiovascular diseases. Results of the quoted studies could have important consequences for the knowledge of risk factors, prevention, or even therapy of many diseases.
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Gnansia, E. Environnement, génétique et épigénétique. Rev. med. perinat. 9, 66–72 (2017). https://doi.org/10.1007/s12611-017-0413-4
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DOI: https://doi.org/10.1007/s12611-017-0413-4