Fibroblast autophagy in fibrotic disorders

Authors

  • Domenico Del Principe,

    1. San Raffaele Institute Sulmona, L'Aquila, Italy
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  • Pasquale Lista,

    1. Department of Therapeutic Research and Medicine Evaluation, Istituto Superiore di Sanità, Rome, Italy
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  • Walter Malorni,

    1. San Raffaele Institute Sulmona, L'Aquila, Italy
    2. Department of Therapeutic Research and Medicine Evaluation, Istituto Superiore di Sanità, Rome, Italy
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  • Anna Maria Giammarioli

    Corresponding author
    1. Department of Therapeutic Research and Medicine Evaluation, Istituto Superiore di Sanità, Rome, Italy
    • Correspondence to:AM Giammarioli, Department of Therapeutic Research and Medicine Evaluation, Section of Degenerative Diseases, Ageing and Gender Medicine, Istituto Superiore di Sanita, Viale Regina Elena 299, 00161 Rome, Italy. e-mail: anna.giammarioli@iss.it

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  • No conflicts of interest were declared.

Abstract

Fibrotic disorders are multistage progressive processes that often arise from different causes and are commonly associated with chronic inflammation. Excessive deposition of extracellular matrix is the hallmark of many fibrotic diseases. This may be due to an excess of fibroblast recruitment and activation, as well as to their differentiation in myofibroblasts. These events may be triggered by cytokines, chemokines and growth factors released by lymphocytes or macrophages. The excessive production of extracellular matrix is apparently due to alterations of metabolic pathways in activated fibroblasts. It has been suggested that a defective autophagy, an important subcellular pathway with multiple homeostatic roles, also recognized as a key component of both innate and acquired immunity, could play a role. In this review we illustrate recent insights in the field, suggesting the possible implication of the immune system in orchestrating the fibrotic response via the modulation of autophagic pathways.

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