Синдромът на обструктивна сънна апнея (СОСА) се проявява с повтарящи се епизоди на частично (хипопнея) или пълно (апнея) прекъсване на дишането по време на сън1-4. Сънната апнея често се съпровожда (или се предизвиква) от обезитас (натрупана и възпалена адипозна тъкан, от която се секретират проинфламаторни медиатори). Друга коморбидност на СОСА е метаболитен синдром и други сърдечно-метаболитни болести2-4. Тази клинична „симбиоза“ провокира провеждането на експериментални и клинични изследвания за участието на адипокини в патогенезата и усложненията на СОСА; адипокините са мултифункционални протеини, секретирани от адипоцити и други клетки на адипозната тъкан5-8. На молекулно равнище СОСА може да бъде номиниран за списъка на low grade inflammationdisorders, в който активно участва дисбалансът на секрецията на про- и анти-инфламаторни адипокини (Фиг. 1).
Примери за адипокини и СОСА:
- Лептин4, 7-9, 11, 13, Адипонектин7, 8, 10, 11, 13
- Резистин7, 8, 12, 13, Hypoxia-induciblefactor-18
- Nеrve growth factor16, 17, Brain-derived neurotrophic factor16-24
- Висфатин25, Interleukin-6, Monocyte chemoattractant protein-1
- Plasminogen activator inhibitor-126
- C-Reactive protein, Tumor necrosis factor-α (27)
- Chemerin28, Obestatin, Apelin29
Интересно е, че nasal continuous positive airway pressure (nCPAP), сравнително най-доброто нехирургично лечение на СОСА, възстановява секреторната хомеостаза на адипозната тъкан.
Фиг. 1. Адипозна дисфункция в патобиологията на СОСА. Оксидативен стрес, „фрагментирана“ хипоксия, повишена активност на симпатикови нерви и възпаление водят до адипозна дисфункция, която променя секрецията на адипокини и те участват в развитието на СОСА и свързаните с него сърдечнометаболитни и когнитивни нарушения.Това е circulos viciosos, в който попада СОСА. (Тази фигура е от (8)).
Литература:
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