Extracellular vesicles: Playing a Role in the Widespread Dispersion of Scleroderma-Induced Fibrosis

Previous studies Extracellular vesicles: Playing a Role in the Widespread Dispersion of Scleroderma-Induced Fibrosis
Extracellular vesicles: Playing a Role in the Widespread Dispersion of Scleroderma-Induced Fibrosis

Extracellular vesicles: Playing a Role in the Widespread Dispersion of Scleroderma-Induced Fibrosis


Extracellular vesicles (EVs) are small membrane-bound structures released by cells that play a critical role in intercellular communication. They act as carriers of various bioactive molecules such as proteins, nucleic acids, and lipids, allowing for the transfer of information between cells. Recent research has uncovered the involvement of EVs in the development and progression of various diseases, including cancer, neurodegenerative disorders, and autoimmune conditions. In the context of scleroderma-induced fibrosis, EVs have emerged as key players in the widespread dispersal of fibrotic signals throughout the body.

Understanding Scleroderma-Induced Fibrosis

Scleroderma, or systemic sclerosis, is a chronic autoimmune disease characterized by excessive fibrosis in various tissues and organs. One of the most debilitating manifestations of scleroderma is fibrosis, the abnormal accumulation of extracellular matrix components such as collagen, leading to tissue stiffness and organ dysfunction. The underlying cause of fibrosis in scleroderma remains poorly understood, but recent studies have implicated EVs in its development and progression.

The Role of Extracellular Vesicles

EVs have been shown to play a dual role in fibrosis. On one hand, they contribute to the activation of fibroblasts, the primary cells responsible for producing collagen and other components of the extracellular matrix. EVs derived from activated immune cells or injured tissues carry pro-fibrotic molecules such as transforming growth factor-beta (TGF-β) and platelet-derived growth factor (PDGF), which stimulate fibroblasts to increase collagen synthesis. Furthermore, EVs can induce a phenotypic switch in fibroblasts, causing them to transform into myofibroblasts, which are highly contractile cells that secrete large amounts of collagen.

On the other hand, EVs are involved in the dispersal of fibrotic signals throughout the body. These vesicles can travel through various bodily fluids, including blood, lymph, and synovial fluid, allowing them to reach distant tissues and organs. Therefore, EVs can contribute to the systemic nature of scleroderma by disseminating pro-fibrotic molecules to remote sites. This widespread dispersion of fibrotic signals further amplifies fibrosis and contributes to the progression of the disease.

Previous Studies

Previous studies have provided valuable insights into the role of EVs in scleroderma-induced fibrosis. One study demonstrated that EVs derived from scleroderma patients contain increased levels of pro-fibrotic molecules compared to healthy individuals. These EVs were also found to stimulate the migration and differentiation of fibroblasts, promoting fibrosis. Another study investigated the impact of EVs on the pulmonary fibrosis commonly observed in scleroderma patients. The researchers found that EVs derived from lung fibroblasts induced the differentiation of resident fibroblasts into myofibroblasts, highlighting their role in the pathogenesis of pulmonary fibrosis.

Targeting Extracellular Vesicles as a Therapeutic Strategy

Given the significant contribution of EVs to scleroderma-induced fibrosis, targeting these vesicles presents a promising therapeutic strategy. Several approaches have been proposed to modulate EV release or interfere with their cargo. One potential approach is the use of inhibitors that target key molecular pathways involved in EV biogenesis or release. Additionally, researchers are exploring the use of engineered EVs that can be loaded with anti-fibrotic molecules and delivered specifically to sites of fibrosis. These therapeutic EVs could counteract the pro-fibrotic signals and promote the resolution of fibrosis.


Extracellular vesicles play a critical role in the widespread dispersion of scleroderma-induced fibrosis. These vesicles serve as vehicles for the transfer of pro-fibrotic molecules, contributing to the activation of fibroblasts and the dissemination of fibrotic signals to remote tissues and organs. Understanding the involvement of EVs in scleroderma holds great potential for the development of targeted therapies. By targeting the release or cargo of EVs, it may be possible to modulate fibrotic signals and alleviate the burden of fibrosis in scleroderma patients.


1. Are extracellular vesicles unique to scleroderma-induced fibrosis?

No, extracellular vesicles are involved in various diseases and biological processes. However, their role in scleroderma-induced fibrosis is increasingly being recognized and studied.

2. How are extracellular vesicles released from cells?

Extracellular vesicles are released by cells through various mechanisms, including the budding of vesicles from the plasma membrane and the trafficking of intracellular vesicles to the cell surface for release.

3. Can targeting extracellular vesicles have broader implications beyond scleroderma-induced fibrosis?

Yes, targeting extracellular vesicles has the potential to be a therapeutic strategy for other fibrotic conditions and diseases characterized by dysregulated intercellular communication. Further research is needed to explore their broader implications.[3]

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