Senescence in the lung: is this getting old?

Morty, Rory E.; Prakash, Y. S.

doi:10.1152/ajplung.00081.2019

Cited by 13 publications

(9 citation statements)

References 61 publications

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“…But with accumulating in vivo evidence including the presence of senescence in aged human skin cells [3], scientists accepted senescence as a true biological phenomenon. Senescence is now known to contribute to a variety of age-related diseases including: type 2 diabetes, obesity, atherosclerosis, chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, and others [4][5][6]. With aging, our cells continually divide, shorten their telomeres, accumulate mutations and DNA damage, all of which ultimately increase the likelihood of oncogenesis [7,8].…”

mentioning

confidence: 99%

Cellular senescence: friend or foe to respiratory viral infections?

2020

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Cellular senescence permanently arrests the replication of various cell types and contributes to age-associated diseases. In particular, cellular senescence may enhance chronic lung diseases including chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. However, the role cellular senescence plays in the pathophysiology of acute inflammatory diseases, especially viral infections, is less well-understood. There is evidence that cellular senescence prevents viral replication by increasing antiviral cytokines, but other evidence shows that senescence may enhance viral replication by downregulating antiviral signalling. Furthermore, cellular senescence leads to the secretion of inflammatory mediators, which may either promote host defense or exacerbate immune pathology during viral infections. In this perspective, we summarise how senescence contributes to physiology and disease, the role of senescence in chronic lung diseases, and how senescence impacts acute respiratory viral infections. Finally, we develop a potential framework of how senescence may contribute, both positively and negatively, to the pathophysiology of viral respiratory infections, including SARS-CoV-2.

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confidence: 99%

Cellular senescence: friend or foe to respiratory viral infections?

2020

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“…Abb. 1; [5]). Es ist außerdem auffällig, dass diese Erkrankungen gehäuft gemeinsam auftreten, wenn auch die Einzelfaktoren der Alterung unterschiedliche Schwerpunkt aufweisen [6].…”

Section: Seneszenz In Der Pathogenese Der Idiopathischen Lungenfibroseunclassified

Alterung von Lunge und Immunsystem als Meilensteine in der Pathogenese von idiopathischer Lungenfibrose und COVID-19

Stieglitz

Frohnhofen

2021

Pneumologe

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“…Severe COVID-19 illness and death is more common in people aged 60 and older with underlying conditions, which can include chronic respiratory system disease not only due to chronic exposure to PM air pollution but also to immuno-senescence and inflamm-aging phenomena [18][19][20][21][22]. Given the linkage between mitochondria functionality, ion channels including CRAC, and inflamm-aging [23], the ability of metformin to target mitochondrial electron transport and prevent ROS/CRACmediated IL-6 release might illuminate a preventive (and prophylactic) measure to quell the raging of the cytokine and thrombotic-like storms that are the leading causes of COVID-19 morbidity and mortality in older people.…”

Section: Cov-2 Infectionmentioning

confidence: 99%

Metformin and SARS-CoV-2: mechanistic lessons on air pollution to weather the cytokine/thrombotic storm in COVID-19

Menéndez

2020

Aging

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Particulate matter air pollution and SARS-CoV-2/COVID-19: A mechanistically linked pathway illuminating a therapeutic opportunity for metforminParticulate matter (PM) air pollution concentrations frequently encountered in major cities can trigger the release of proinflammatory interleukins (e.g., IL-6) from alveolar macrophages, promoting an acceleration of arterial thrombosis [1]. Analogously, infection with the novel SARS-CoV-2 coronavirus can stimulate a too-littletoo-late type-I interferon-mediated innate immune response, which is inherently accompanied by dysregulated secretion of IL-6 from alveolar macrophages [2,3]. The so-called cytokine storminvolving overproduction of proinflammatory cytokines and overactivation of immune cells (hyperinflammation)ultimately drives an acute respiratory distress syndrome (ARDS), one of the leading causes of mortality in patients with severe COVID-19 disease [4,5]. Intriguingly, patients with severe COVID-19 admitted to the intensive care unit are at highest thrombotic risk, with acute pulmonary embolism being the most common thrombotic complication [6]. The ability of COVID-19 to predispose to thromboembolism, which can fuel futile cycles of hyperinflammatory responses that aggravate SARS-CoV-2 pathogenesis [7,8], is increasingly viewed as a major factor in disease severity and mortality. It is thus not surprising that long-term exposure to PM has been recently proposed as a key contributor to COVID-19 mortality in the United States [9]. Likewise, the elevated levels of PM air pollution in Northern Italy and central Spain have been postulated as a putative risk factor underlying the extremely high COVID-19 fatality rates observed in these European regions [10][11][12].

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Senescence in the lung: is this getting old?

Cited by 13 publications

References 61 publications

Cellular senescence: friend or foe to respiratory viral infections?

Cellular senescence: friend or foe to respiratory viral infections?

Alterung von Lunge und Immunsystem als Meilensteine in der Pathogenese von idiopathischer Lungenfibrose und COVID-19

Metformin and SARS-CoV-2: mechanistic lessons on air pollution to weather the cytokine/thrombotic storm in COVID-19

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