Update in Environmental and Occupational Medicine 2010

Budinger, G. R. Scott; Mutlu, Gökhan M.

doi:10.1164/rccm.201103-0467up

Cited by 13 publications

(8 citation statements)

References 62 publications

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“…Alveolar epithelial cell apoptosis was found as major underlying cause of severe lung parenchymal damage in sterile or infectious lung injury (Albertine et al, 2002; Herold et al, 2008; Ma et al, 2010; Budinger et al, 2011). Re-epithelialization (given an intact basement membrane) and endothelial re-sealing following bronchoalveolar injury is considered as critical step to re-establish normal gas exchange conditions in the lung.…”

Section: Lung Macrophages In Tissue Repair and Remodelingmentioning

confidence: 99%

Acute Lung Injury: How Macrophages Orchestrate Resolution of Inflammation and Tissue Repair

Herold¹,

Mayer²,

Lohmeyer³

2011

Front. Immun.

281

310

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Lung macrophages are long living cells with broad differentiation potential, which reside in the lung interstitium and alveoli or are organ-recruited upon inflammatory stimuli. A role of resident and recruited macrophages in initiating and maintaining pulmonary inflammation in lung infection or injury has been convincingly demonstrated. More recent reports suggest that lung macrophages are main orchestrators of termination and resolution of inflammation. They are also initiators of parenchymal repair processes that are essential for return to homeostasis with normal gas exchange. In this review we will discuss cellular cross-talk mechanisms and molecular pathways of macrophage plasticity which define their role in inflammation resolution and in initiation of lung barrier repair following lung injury.

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Section: Lung Macrophages In Tissue Repair and Remodelingmentioning

confidence: 99%

Acute Lung Injury: How Macrophages Orchestrate Resolution of Inflammation and Tissue Repair

Herold¹,

Mayer²,

Lohmeyer³

2011

Front. Immun.

281

310

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“…In pediatric asthma patients, Strickland et al found that short-term exposure to air pollutants increased the number of emergency department visits, even with exposure at relatively low concentrations [3]. Desert dust, which is considered to be harmless, can increase the prevalence of asthma and the occurrence of asthma symptoms [4][5][6]. Asian dust storms (ADS) originating in the deserts of Mongolia, northern China, and Kazakhstan often disperse dust over East Asia from spring until late autumn.…”

Section: Introductionmentioning

confidence: 99%

Effects on asthma and induction of interleukin-8 caused by Asian dust particles collected in western Japan

Watanabe

Kurai

Tomita³

et al. 2014

Journal of Asthma

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“…The proper maintenance of homeostatic balance is essential for cell survival in a constantly changing environment. Human pulmonary tissue forms an interface between the external and internal microenvironments, and is therefore constantly exposed to both exogenous stressors including combustion products (diesel exhaust, carbon monoxide, cigarette smoke (CS)), particulate matter, ozone, [5][6][7] and endogenous stressors (eg, mitochondrial-derived reactive oxygen species (ROS), unfolded proteins, nutrient deprivation), all of which can alter cellular homeostasis. Pulmonary cells are equipped with a variety of defense mechanisms to aid in the preservation of cellular homeostasis in the face of such harsh conditions [8][9][10] as outlined in one of our previous network model describing the main CS-related cellular stress defense mechanisms in detail.…”

Section: Introductionmentioning

confidence: 99%

Construction of a Computable Network Model for DNA Damage, Autophagy, Cell Death, and Senescence

Gebel

Lichtner

Frushour

et al. 2013

Bioinform Biol Insights

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Towards the development of a systems biology-based risk assessment approach for environmental toxicants, including tobacco products in a systems toxicology setting such as the “21st Century Toxicology”, we are building a series of computable biological network models specific to non-diseased pulmonary and cardiovascular cells/tissues which capture the molecular events that can be activated following exposure to environmental toxicants. Here we extend on previous work and report on the construction and evaluation of a mechanistic network model focused on DNA damage response and the four main cellular fates induced by stress: autophagy, apoptosis, necroptosis, and senescence. In total, the network consists of 34 sub-models containing 1052 unique nodes and 1538 unique edges which are supported by 1231 PubMed-referenced literature citations. Causal node-edge relationships are described using the Biological Expression Language (BEL), which allows for the semantic representation of life science relationships in a computable format. The Network is provided in .XGMML format and can be viewed using freely available network visualization software, such as Cytoscape.

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Update in Environmental and Occupational Medicine 2010

Cited by 13 publications

References 62 publications

Acute Lung Injury: How Macrophages Orchestrate Resolution of Inflammation and Tissue Repair

Acute Lung Injury: How Macrophages Orchestrate Resolution of Inflammation and Tissue Repair

Effects on asthma and induction of interleukin-8 caused by Asian dust particles collected in western Japan

Construction of a Computable Network Model for DNA Damage, Autophagy, Cell Death, and Senescence

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