Rejuvenating cellular respiration for optimizing respiratory function: targeting mitochondria

Agrawal, Anurag; Mabalirajan, Ulaganathan

doi:10.1152/ajplung.00320.2015

Cited by 65 publications

(73 citation statements)

References 127 publications

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“…One potential clue is that mitochondrial CaMKII inhibition is protective in a variety of myocardial injury models linked to elevated ROS and mitochondrial dysfunction (7,20,55,56). Here, we show increased levels of ox-CaMKII in the mitochondria of murine lung homogenates and primary HAEC after allergen challenge, while inhibition of Mt-CaMKII reduced expression and Mt-ROS production.…”

Section: Discussionmentioning

confidence: 68%

“…in asthma; however, sources of these phenomena are unclear (6,7,(10)(11)(12)54). One potential clue is that mitochondrial CaMKII inhibition is protective in a variety of myocardial injury models linked to elevated ROS and mitochondrial dysfunction (7,20,55,56).…”

Section: Discussionmentioning

confidence: 99%

“…Existing treatments, such as bronchodilators and steroids, alleviate symptoms without selectively targeting specific pathologic mediators (2,3). While numerous studies have provided evidence that asthma is a pleiotropic disease marked by increased airway ROS, the molecular mechanisms that connect ROS to asthma phenotypes are uncertain (4)(5)(6)(7). We recently made the unanticipated discovery that the multifunctional Ca 2+ /calmodulin-dependent protein kinase II (CaM-KII) in airway epithelium is a key regulator of the ROS-linked asthmatic phenotypes of inflammation, eosinophilic recruitment and infiltration, and airway hyperreactivity (AHR) in murine models of allergic asthma (8).…”

Section: Introductionmentioning

confidence: 99%

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Mitochondrial CaMKII inhibition in airway epithelium protects against allergic asthma

et al. 2017

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Section: Discussionmentioning

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mitochondrial CaMKII inhibition in airway epithelium protects against allergic asthma

et al. 2017

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“…Therefore, the presence of O 2 − plays an important role in the formation of other forms of ROS. Excessive levels of mitochondrial ROS degrade the mitochondrial function and lead to the collapse of electrochemical gradient, which leaves the cell more susceptible to ROS-mediated injury 35. Given that oxidative stress in COPD patients is a prevailing phenomenon, we next reviewed how oxidative stress induced by excessive ROS plays a role in the pathogenesis of inflammation in COPD.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial alterations during oxidative stress in chronic obstructive pulmonary disease

Jiang¹,

Wang²,

Hu³

2017

COPD

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The high incidence of chronic obstructive pulmonary disease (COPD), one of the most prevalent diseases worldwide, has attracted growing attention. Cigarette smoking is considered a major contributory factor in the pathogenesis and progression of COPD due to the tremendous oxidative burden that it causes, which induces an oxidant/antioxidant imbalance. Excessive oxidation induced by the excessive generation of mitochondrial reactive oxygen species disturbs the antioxidant systems and plays an important role in triggering and promoting chronic inflammation of airways. Given that mitochondria is one of the main sites of reactive oxygen species production by the oxidative phosphorylation process, oxidative stress may affect mitochondrial function by changing its structure and morphology and by affecting a series of mitochondrial proteins. In particular, PTEN-induced putative kinase 1/Parkin and p62 play critical roles in mitophagy. During the process, the Akt ubiquitin E3 ligase is an important mediator associated with cigarette smoke exposure-induced pulmonary endothelial cell death and dysfunction. Thus, understanding the underlying mechanisms of the signaling pathway may provide important information regarding the therapeutic treatment of COPD by application of alternative PTEN-induced putative kinase 1 targets or ubiquitin E3 ligase.

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“…In addition to mitochondrial genetic disease (51), altered biogenesis and mitochondrial exhaustion is the leading cause of several oxidative disorders, including Chronic obstructive pulmonary disease (COPD) and aging related degenerative pathologies (52). Beneficial effects of mitochondrial transfer are observed in ischemic perfusion model and in metastatic cancer cells (53).…”

Section: Introductionmentioning

confidence: 99%

Stromal Progenitor Cells in Mitigation of Non-hematopoietic Radiation Injuries

Kulkarni

Wang²,

Guha

2016

Curr Pathobiol Rep

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Purpose of review Therapeutic exposure to high doses of radiation can severely impair organ function due to ablation of stem cells. Normal tissue injury is a dose-limiting toxicity for radiation therapy (RT). Although advances in the delivery of high precision conformal RT has increased normal tissue sparing, mitigating and therapeutic strategies that could alleviate early and chronic radiation effects are urgently needed in order to deliver curative doses of RT, especially in abdominal, pelvic and thoracic malignancies. Radiation-induced gastrointestinal injury is also a major cause of lethality from accidental or intentional exposure to whole body irradiation in the case of nuclear accidents or terrorism. This review examines the therapeutic options for mitigation of non-hematopoietic radiation injuries. Recent findings We have developed stem cell based therapies for the mitigation of acute radiation syndrome (ARS) and radiation-induced gastrointestinal syndrome (RIGS). This is a promising option because of the robustness of standardized isolation and transplantation of stromal cells protocols, and their ability to support and replace radiation-damaged stem cells and stem cell niche. Stromal progenitor cells (SPC) represent a unique multipotent and heterogeneous cell population with regenerative, immunosuppressive, anti-inflammatory, and wound healing properties. SPC are also known to secrete various key cytokines and growth factors such as platelet derived growth factors (PDGF), keratinocyte growth factor (KGF), R-spondins (Rspo), and may consequently exert their regenerative effects via paracrine function. Additionally, secretory vesicles such as exosomes or microparticles can potentially be a cell-free alternative replacing the cell transplant in some cases. Summary This review highlights the beneficial effects of SPC on tissue regeneration with their ability to (a) target the irradiated tissues, (b) recruit host stromal cells, (c) regenerate endothelium and epithelium, (d) and secrete regenerative and immunomodulatory paracrine signals to control inflammation, ulceration, wound healing and fibrosis.

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Rejuvenating cellular respiration for optimizing respiratory function: targeting mitochondria

Cited by 65 publications

References 127 publications

Mitochondrial CaMKII inhibition in airway epithelium protects against allergic asthma

Mitochondrial CaMKII inhibition in airway epithelium protects against allergic asthma

Mitochondrial alterations during oxidative stress in chronic obstructive pulmonary disease

Stromal Progenitor Cells in Mitigation of Non-hematopoietic Radiation Injuries

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