antifibrotika

Antifibrotika are substances or drugs designed to reduce or prevent fibrosis, the excessive accumulation of connective tissue that can lead to organ dysfunction. They aim to interrupt the activation and proliferation of fibroblasts and the deposition of extracellular matrix, thereby slowing or halting the fibrotic process in affected tissues.

Mechanisms of action vary and often target key fibrogenic pathways. Many antifibrotics seek to modulate transforming growth factor-beta signaling, inflammatory mediators, and growth factor receptors involved in fibroblast activation. Some also influence collagen synthesis, matrix remodeling, or angiogenesis. Because fibrosis involves multiple cell types and pathways, antifibrotics may have broad or tissue-specific effects.

The most established antifibrotic drugs are pirfenidone and nintedanib. Both are approved for idiopathic pulmonary fibrosis (IPF) and for a range of progressive fibrosing interstitial lung diseases. In clinical trials, they slow the decline in lung function, as measured by forced vital capacity, and may reduce the rate of disease progression. Pirfenidone is associated with photosensitivity and gastrointestinal symptoms, and requires monitoring of liver enzymes. Nintedanib commonly causes gastrointestinal side effects and is also monitored for liver function.

Beyond IPF, research investigates antifibrotics in hepatic fibrosis, liver cirrhosis, and other organ fibroses, including agents targeting bile acid pathways, collagen cross-linking, or multiple pro-fibrotic signals. While antifibrotics can slow progression, they are not cures, and effectiveness varies by disease and patient.

Overall, antifibrotika represent a therapeutic class aimed at modifying disease biology rather than merely treating symptoms, with ongoing research to expand indications and improve safety.