Фіброгенез у підшлунковій залозі: сучасні уявлення
DOI:
https://doi.org/10.30978/MG-2019-4-67Ключові слова:
підшлункова залоза, зірчасті клітини, фіброз, позаклітинний матрикс, сигнальні шляхи, перспективи антифібротичної терапіїАнотація
Панкреатичні зірчасті клітини становлять собою плюрипотентні клітини, розташовані між часточками підшлункової залози та ацинусів, що їх оточують. У стані спокою (неактивованому стані) панкреатичні зірчасті клітини містять у цитоплазмі запас вітаміну А (ретиноїдів), проміжні філаменти, десмін, гліофібрилярний кислий білок, нестин, нейроектодермальні білки, молекули адгезії нервових клітин і фактор росту нервів. Після активації панкреатичні зірчасті клітини можуть трансформуватися в міофібробластоподібні клітини. Вони втрачають ліпідні краплі з вітаміном A, в них зменшується вміст віментину, десміну. Підвищується проліферація, міграція, збільшується синтез внутрішньоклітинного матриксу. Доказові дані свідчать про те, що активовані панкреатичні зірчасті клітини є основним джерелом накопичення білка позаклітинного матриксу при патологічних станах, які призводять до фіброзу в підшлунковій залозі при хронічному панкреатиті та раку підшлункової залози. Проаналізовано сучасні дані літератури щодо механізмів фіброзу підшлункової залози та ролі зірчастих клітин у фіброгенезі. Наведено результати досліджень функції панкреатичних зірчастих клітин у нормі та за патології (при гострому і хронічному панкреатиті, раку підшлункової залози). Описано варіанти фіброзу підшлункової залози, механізми його розвитку при старінні. Узагальнено результати недавніх досліджень біологічних властивостей панкреатичних зірчастих клітин, зокрема їх участь у синтезі екзосом, процесах клітинного старіння, епітеліальної мезенхімальної трансформації, метаболізмі. Особливе значення має розробка антифібротичної терапії на основі теоретичних знань і результатів експериментальних досліджень.Посилання
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