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Journal ArticleDOI

Premature lung aging and cellular senescence in the pathogenesis of idiopathic pulmonary fibrosis and COPD/emphysema.

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TLDR
According to recently proposed pathogenic models in COPD and IPF, premature cellular senescence likely affects distinct progenitors cells, leading to stem cell exhaustion, with emphasis on the possible molecular and cellular mechanisms leading to the severe parenchymal remodeling that characterizes, in different ways, these deadly diseases.
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This article is published in Translational Research.The article was published on 2013-09-01. It has received 261 citations till now. The article focuses on the topics: Premature aging & Idiopathic pulmonary fibrosis.

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Journal ArticleDOI

Cellular senescence: from physiology to pathology.

TL;DR: In cancer and during active tissue repair, pro-senescent therapies contribute to minimize the damage by limiting proliferation and fibrosis, respectively, and antisenescent therapies may help to eliminate accumulated senescent cells and to recover tissue function.
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Cellular senescence in aging and age-related disease: from mechanisms to therapy

TL;DR: Current progress and challenges in understanding the stressors that induce senescence in vivo, the cell types that are prone to senesce, and the autocrine and paracrine properties of senescent cells in the contexts of aging and age-related diseases as well as disease therapy are discussed.
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The Continuum of Aging and Age-Related Diseases: Common Mechanisms but Different Rates.

TL;DR: The hypothesis that ARDs and GSs such as frailty can be conceptualized as accelerated aging will be discussed, and the use of DNA methylation, N-glycans profiling, and gut microbiota composition to complement the available disease-specific markers are proposed.
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Identification of HSP90 inhibitors as a novel class of senolytics

TL;DR: Treatment of Ercc1−/∆ mice, a mouse model of a human progeroid syndrome, with the HSP90 inhibitor 17-DMAG extended healthspan, delayed the onset of several age-related symptoms and reduced p16INK4a expression, demonstrating the utility of a senescence associated β-galactosidase assay as a screening platform to rapidly identify drugs that specifically affect senescent cells.
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Accelerated ageing of the lung in COPD: new concepts

TL;DR: Evidence is discussed showing how oxidative stress induces accelerated ageing by upregulating the phosphatidylinositol-4,5-bisphosphate 3-kinase/AKT/mechanistic target of rapamycin signalling pathway resulting in depletion of stem cells, defective autophagy, reduced antioxidant responses and defective mitochondrial function thus generating further oxidative stress.
References
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Journal ArticleDOI

Epithelial-Mesenchymal Transitions in Development and Disease

TL;DR: The mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis.
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Identification of c-MYC as a Target of the APC Pathway

TL;DR: The c-MYC oncogene is identified as a target gene in this signaling pathway and shown to be repressed by wild-type APC and activated by beta-catenin, and these effects were mediated through Tcf-4 binding sites in the c- MYC promoter.
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Human mesenchymal stem cells modulate allogeneic immune cell responses

Sudeepta Aggarwal, +1 more
- 15 Feb 2005 - 
TL;DR: Insight is offered into the interactions between allogeneic MSCs and immune cells and mechanisms likely involved with the in vivo MSC-mediated induction of tolerance that could be therapeutic for reduction of GVHD, rejection, and modulation of inflammation.
Journal ArticleDOI

The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression

TL;DR: A senescence-associated secretory phenotype (SASP) is acquired that turns senescent fibroblasts into proinflammatory cells that have the ability to promote tumor progression.
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