Proapoptotic Bid is required for pulmonary fibrosis

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Proapoptotic Bid is required for pulmonary fibrosis.

The molecular mechanisms of pulmonary fibrosis are poorly understood. Previous reports indicate that activation of TGF-beta1 is essential for the development of pulmonary fibrosis. Here, we report that the proapoptotic Bcl-2 family member Bid is required for the development of pulmonary fibrosis after the intratracheal instillation of bleomycin. Mice lacking Bid exhibited significantly less pul...

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Proapoptotic BID is required for myeloid homeostasis and tumor suppression.

The proper expansion and contraction of hematopoietic cells requires tight regulation of cell death. BID, a "BH3-only" molecule, amplifies death receptor signals connecting the extrinsic to intrinsic pathways by triggering the mitochondrial pathway of apoptosis. Bid-deficient mice, as they age, spontaneously develop a myeloproliferative disorder, which progresses from myeloid hyperplasia to a f...

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A Role for Proapoptotic BID in the DNA-Damage Response

The BCL-2 family of apoptotic proteins encompasses key regulators proximal to irreversible cell damage. The BH3-only members of this family act as sentinels, interconnecting specific death signals to the core apoptotic pathway. Our previous data demonstrated a role for BH3-only BID in maintaining myeloid homeostasis and suppressing leukemogenesis. In the absence of Bid, mice accumulate chromoso...

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Background and Objectives: Idiopathic pulmonary fibrosis (IPF) is characterized by progressively worsening lung function, ventilation capacity, dyspnea, and finally reduced exercise intolerance. All of these have a significant negative impact on functional capacity and quality of life. In this study, we aim to evaluate the effects of pulmonary rehabilitation (PR) in IPF and assess the predictor...

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Idiopathic pulmonary fibrosis is the most devastating diffuse fibrosing lung disease of unknown aetiology. Compelling evidence suggests that both protease-activated receptor (PAR)-1 and PAR-2 participate in the development of pulmonary fibrosis. Previous studies have shown that bleomycin-induced lung fibrosis is diminished in both PAR-1 and PAR-2 deficient mice. We thus have been suggested that...

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ژورنال

عنوان ژورنال: Proceedings of the National Academy of Sciences

سال: 2006

ISSN: 0027-8424,1091-6490

DOI: 10.1073/pnas.0507604103