Fibrosis

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Fibrosis
Synonyms
Pronounce
Field Pathology, rheumatology
Symptoms Often asymptomatic;
can vary based on the affected organ
Complications Cirrhosis, organ dysfunction,
loss of organ function
Onset Can be congenital or acquired
Duration Chronic or progressive
Types Depending on the affected tissue or organ
Causes Chronic inflammation, repeated injury,
genetic predispositions
Risks Chronic diseases, radiation exposure,
certain medications, environmental toxins
Diagnosis Biopsy, imaging techniques,
laboratory tests
Differential diagnosis Other conditions causing
organ dysfunction or scarring
Prevention Control of inflammation,
avoidance of causative agents, genetic counseling
Treatment Depends on cause and location;
may include medications, therapy, or surgery
Medication Anti-inflammatory drugs,
antifibrotic agents, enzyme replacements
Prognosis Varies; can be benign or
lead to severe organ dysfunction
Frequency Varies based on type and cause
Deaths Depends on severity and organ involvement


Fibrosis is the pathological accumulation of excess fibrous connective tissue in organs or tissues as a reparative or reactive process.[1] While it can be a reactive or benign state, pathological fibrosis can severely compromise the function of the affected organ. The process may be termed scarring when it follows injury. Fibrosis that arises from a single cell line is labeled a fibroma. Essential to the wound healing process, fibrosis can nevertheless disrupt the normal architecture and function of the underlying organ or tissue when excessive.[2] Predominantly characterized by the excessive accumulation of extracellular matrix (ECM) proteins, fibrosis essentially represents an overzealous wound healing response that can significantly hinder normal organ function.[3]

Physiology[edit | edit source]

The physiological mechanisms underlying fibrosis bear a close resemblance to those of scarring; both processes involve the deposition of connective tissue by stimulated fibroblasts. Initiating factors often include soluble substances released by immune cells, such as macrophages. TGF beta, the most extensively studied pro-fibrotic mediator, is secreted by macrophages and the interstitium in damaged tissues. Other key soluble fibrosis mediators encompass CTGF, platelet-derived growth factor (PDGF), and interleukin 10 (IL-10). These molecules activate intricate signal transduction pathways, notably the AKT/mTOR[4] and SMAD[5] pathways, which stimulate fibroblast proliferation and activation, ultimately leading to the deposition of extracellular matrix in the surrounding connective tissue. Although vital for tissue repair, if this process becomes deregulated or encounters repetitive or severe tissue injuries, it can culminate in a progressive, irreversible fibrotic response.[3]

Anatomical location[edit | edit source]

Fibrosis manifests in multiple body tissues, often as a result of damage or inflammation. The following are common examples:

Lungs

Liver

Heart

Brain

Other Tissues and Organs

Incidence[edit | edit source]

Recent studies have highlighted the increasing incidence of fibrosis in various conditions. For instance, liver fibrosis due to chronic hepatitis C infection has emerged as a significant healthcare issue in several countries.[6] Also, idiopathic pulmonary fibrosis has observed an uptick in incidence in the last two decades, making it a research priority in respiratory medicine.[7]

See also[edit | edit source]

Fibroblast Granuloma Interstitial lung disease Scarring

Fibrosis Resources
Wikipedia


Classification
External resources


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Contributors: Prab R. Tumpati, MD