Exploring the Interplay between Cellular Senescence, Immunity, and Fibrosing Interstitial Lung Diseases (f-ILDs): Challenges and Opportunities

Cellular senescence in fibrosing interstitial lung diseases (f-ILDs)
Discover how cellular senescence, marked by antagonistic pleiotropy, and immune dysregulation play a detrimental role in the pathogenesis of fibrosing interstitial lung diseases (f-ILDs) and pulmonary fibrosis.

Understanding the Role of Cellular Senescence in f-ILDs (Fibrosing Interstitial Lung Diseases)

Fibrosing interstitial lung diseases (ILDs) are characterized by the gradual and irreversible accumulation of scar tissue in the lung parenchyma.

The role of the immune response in the pathogenesis of pulmonary fibrosis remains unclear. In recent years, substantial advancements have been made in our comprehension of the pathobiology driving fibrosing ILDs, particularly concerning various age-related cellular disturbances and immune mechanisms believed to contribute to an inadequate response to stress and increased susceptibility to lung fibrosis.

Methods:

Emerging studies emphasize cellular senescence as a key mechanism implicated in the pathobiology of age-related diseases, including pulmonary fibrosis.

Results:

Cellular senescence, marked by antagonistic pleiotropy, and the complex interplay with immunity, are pivotal in comprehending many aspects of lung fibrosis.

How Cellular Senescence Contributes to Immune Dysregulation and f-ILDs: Key Findings

Here, we review progress in novel concepts in cellular senescence, its association with the dysregulation of the immune response, and the evidence underlining its detrimental role in fibrosing ILDs.

Authors

Fernanda Hernandez-Gonzalez, Federico Pietrocola, Paolo Cameli, Elena Bargagli, Sergio Prieto-González, Tamara Cruz, Nuria Mendoza, Mauricio Rojas, Manuel Serrano, Alvar Agustí, Rosa Faner, Jose A. Gómez-Puerta and Jacobo Sellares

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Fecha de publicación

Available online 2 September 2024

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