# Fibrosis

Fibrosis is scarring gone overboard. When a tissue is injured, inflamed, or full of senescent cells, specialized cells called myofibroblasts lay down too much connective tissue (mostly collagen types I and III). That stiff, poorly supplied scar replaces healthy working tissue. The chief instigator is a signaling molecule called TGF-beta1. It works through messengers (SMAD2/3) to crank up collagen, block the enzymes that break it down (MMPs), and turn ordinary fibroblasts into scar-forming myofibroblasts. Other players (IL-11, PDGF, and CTGF) pitch in depending on the tissue. Aging makes it worse. As you get older, your body clears senescent cells poorly, so TGF-beta and SASP signals keep flowing, immune cells shift toward a scar-promoting mode, and repair gets messy. That is why liver cirrhosis, lung fibrosis, and heart fibrosis are major causes of age-related organ failure.

## Sources

- Wynn & Ramalingam. (2012). Mechanisms of fibrosis: therapeutic translation for fibrotic disease. Nature Medicine. https://doi.org/10.1038/nm.2807
- Schafer et al.. (2017). Cellular senescence mediates fibrotic pulmonary disease. Nature Communications. https://doi.org/10.1038/ncomms14532

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_Canonical: https://longevity-switzerland.com/en/glossary/fibrosis · Part of Longevity Cities · Updated 2026-06-22_