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In summary, it appears that mitochondria are altered in BD, even before clinical symptoms arise

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(3) Thrombus-responsive biomimetic nanoparticles (PTPN) co-deliver tissue plasminogen activator, phenylboronic acid, and protocatechualdehyde

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Overall, HT pathogenesis results from a complex interplay between innate and adaptive immunity, where breakdowns in tolerance, skewed Th1/Th17/Treg balance, and persistent autoantibody production sustain chronic inflammation and irreversible thyroid destruction

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2010;78(3):S3940

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