The DOI matches its Crossref record; 152 of the 152 references it cites were found in a registry or an index; 9 of the 184 sources its claims cite were checked for support.
Aging and Lung Disease
Open accessAbstract
People worldwide are living longer, and it is estimated that by 2050, the proportion of the world's population over 60 years of age will nearly double. Natural lung aging is associated with molecular and physiological changes that cause alterations in lung function, diminished pulmonary remodeling and regenerative capacity, and increased susceptibility to acute and chronic lung diseases. As the aging population rapidly grows, it is essential to examine how alterations in cellular function and cell-to-cell interactions of pulmonary resident cells and systemic immune cells contribute to a higher risk of increased susceptibility to infection and development of chronic diseases, such as chronic obstructive pulmonary disease and interstitial pulmonary fibrosis. This review provides an overview of physiological, structural, and cellular changes in the aging lung and immune system that facilitate the development and progression of disease.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
This review synthesizes how normal lung aging and immunosenescence alter pulmonary structure, cellular repair, and immune responses, increasing susceptibility to COPD, IPF, ARDS, pneumonia, and asthma exacerbations. It emphasizes that senescence, oxidative stress, ECM remodeling, and innate/adaptive immune dysfunction converge to impair lung homeostasis and disease outcomes.
Key findings
- Natural lung aging causes structural and physiologic changes: increased alveolar size and alveolar-capillary surface area, reduced elastic recoil, increased functional residual capacity, and declines in FEV1 of approximately 30 mL/year and FVC of approximately 20 mL/year, lowering the FEV1/FVC ratio; total lung capacity does not significantly change with age.
- Cellular aging includes increased bronchoepithelial apoptosis, AEC2 senescence, mitochondrial dysfunction, impaired autophagy, decreased proliferating-to-apoptotic AEC ratio, ECM stiffening with increased collagen and decreased elastin/laminin/fibronectin, endothelial dysfunction, and altered airway smooth muscle markers.
- Immunosenescence includes age-associated declines in alveolar macrophage phagocytosis, impaired dendritic cell antigen phagocytosis and migration, decreased neutrophil CD16 with increased superoxide and impaired phagocytosis, altered NET-mediated killing, reduced NK cell function, decreased naïve T cells with increased memory T cells, and impaired B cell development/repertoire diversity.
- Disease links include COPD sharing aging features but with more disorganized collagen and increased collagen, fibronectin, and laminin; IPF survival of less than five years post diagnosis; severe sepsis mortality of 50–60% in elderly patients; and increased pneumonia susceptibility from impaired clearance and bacterial adhesion.
Methods
- Design: narrative review; no primary experiments or systematic review methodology are described.
- Data or sample: synthesis of published human, murine, and in vitro literature; no original human or animal cohort is analyzed.
- Main analysis: thematic overview of physiologic, structural, cellular, immune, and disease-related changes in the aging lung, with 149 cited references.
Limitations
- The paper states that more detailed mechanistic studies are needed to validate genetic determinants of disease progression, understand interactions between immune and lung cell types, clarify when lung aging begins, and link biologic hallmarks of aging to lung phenotypes and disease progression.
- Evident from the text: as a narrative review, it does not report a systematic search strategy, inclusion criteria, quality appraisal, or primary data, and it synthesizes heterogeneous human, murine, and in vitro findings.
- The paper notes that interpretation of healthy or normal lung function in older persons and disease diagnosis can be problematic because of heterogeneity and variable rates of lung aging; height, gender, weight, and ethnicity partly explain FEV1/FVC differences, and reference standards remain to be fully elucidated.
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Claims the paper makes
89 Not checked yet · 31 Own interpretation · 5 Partly supported · 5 No basis given · 1 Supported · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“An age-associated reduction or delay in cytokine, chemokine, or interferon production in response to stimulation can negatively impact innate immune responses in the lung (110).”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG > Alveolar macrophages.
What the sources say
- Partly supportedcites [110] sourceExperimental — accuracy not yet measured
The Results section reports delayed responses and lower cytokine, chemokine, and interferon production in stimulated PBMCs from older donors. The Discussion suggests these changes could impair immune responses, but the study examined blood cells, not innate immune responses in the lung. No page numbers are available in our copy. (LLM, conf=0.86)
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Further, age-associated changes in genomic instability, telomere shortening, epigenetic alterations, cellular senescence, impaired autophagy, and mitochondrial dysfunction may promote IPF development and progression (3, 12, 62, 84, 88, 89, 116, 145).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Aging and Interstitial Lung Disease
What the sources say
- Partly supportedcites [3] sourceExperimental — accuracy not yet measured
The “Senescence in age-related disease” section says senescent cells drive pulmonary fibrosis, and its reference identifies idiopathic pulmonary fibrosis. The paper also discusses telomere shortening, DNA damage and epigenetic changes as causes of senescence, but the passages do not establish that each of the listed changes—including impaired autophagy and mitochondrial dysfunction—promotes IPF development or progression. (LLM, conf=0.89)
- Not checked yetcites [12] source
- Partly supportedcites [62] sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) describes cellular senescence as age-associated and links it to shortened telomeres and DNA damage. But the paper examines susceptibility to pneumococcal pneumonia and discusses COPD, not IPF development or progression; it does not establish the claimed role for the full list of age-associated changes in IPF. (LLM, conf=0.84)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Age-associated immunosenescence and cellular senescence in response to exposure to cigarette smoke can greatly impact COPD pathogenesis (3, 19, 86).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Chronic Obstructive Pulmonary Disease
What the sources say
- Partly supportedcites [3] sourceExperimental — accuracy not yet measured
In “Impact of senescence on human health” (page unavailable), the paper says that defects in the aging immune system may allow senescent cells to persist and identifies cigarette smoke as a disease-causing stressor affecting lung epithelium. It does not specifically establish that these processes greatly affect COPD pathogenesis; its disease discussion uses other conditions as examples. (LLM, conf=0.85)
- Partly supportedcites [19] sourceExperimental — accuracy not yet measured
The Immunologic changes section describes age-related immune dysregulation and inflammation that may increase vulnerability to environmental exposures and lung injury; the Summary links this to possible accelerated lung-function decline. Our copy does not establish cigarette-smoke-induced cellular senescence or its impact on COPD pathogenesis. (LLM, conf=0.83)
- Not checked yetcites [86] source
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Structural changes, such as subepithelial collagen deposition, goblet cell and mucous gland hyperplasia, as well as ASM hypertrophy and hyperplasia, illustrate that remodeling of airways occurs in asthma patients (98, 99).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Age-Associated Lung Function Decline with Asthma
What the sources say
- Partly supportedcites [98] sourceExperimental — accuracy not yet measured
The airway-remodeling passage (section labeled Abstract; page unavailable) describes asthma-associated subepithelial fibrosis and extracellular-matrix deposition, along with ASM hypertrophy and hyperplasia. It describes mucus gland hypertrophy, not hyperplasia, and does not identify goblet cell hyperplasia or specifically subepithelial collagen deposition. (LLM, conf=0.87)
- Partly supportedcites [99] sourceExperimental — accuracy not yet measured
The Introduction (page not supplied) says that airway smooth muscle may undergo hypertrophy and/or hyperplasia in asthma, and the Conclusions discuss airway remodeling. Our copy does not describe subepithelial collagen deposition or goblet-cell and mucous-gland hyperplasia as features of that remodeling, so it supports only part of the cited sentence. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
In the paper
“There is considerable change in lung structure and function with advancing age (summarized in Supplemental Table 1).”
§ Aging and Lung Disease > STRUCTURAL AND PHYSIOLOGIC CHANGES IN THE AGING LUNG
What the sources say
- Not checked yetcites [6] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Alterations in alveolar depth and acinar airway lumen that occur during compensatory remodeling are associated with advanced age (6).”
§ Aging and Lung Disease > STRUCTURAL AND PHYSIOLOGIC CHANGES IN THE AGING LUNG
What the sources say
- Not checked yetcites [6] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“It is well appreciated that, even in healthy persons, lung function declines starting at the age of 35.”
§ Aging and Lung Disease > STRUCTURAL AND PHYSIOLOGIC CHANGES IN THE AGING LUNG
What the sources say
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Age-associated changes in intrinsic mechanisms that aid in cell regeneration and repair, such as depletion of adult stem cell reservoirs, mitochondrial dysfunction, increased oxidative stress, and telomere shortening, contribute to an inability of lung cells to maintain baseline homeostasis.”
§ Aging and Lung Disease > INTRODUCTION
What the sources say
- Not checked yetcites [3] source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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In the paper
“DNA damage in response to compounds, such as those present in cigarette smoke, as well as telomere shortening due to increased demand for injured airway epithelium repair, can result in disease-related senescence and subsequent generation of a secondary subset of senescent cells (5).”
§ Aging and Lung Disease > INTRODUCTION
What the sources say
- Not checked yetcites [5] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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None of the sources cited for this claim have been checked yet.
In the paper
“A decline in elastic recoil combined with a reduction in the number of elastic attachments of supporting alveoli and increased collagen results in smaller airways closing at higher lung volumes (9, 10).”
§ Aging and Lung Disease > STRUCTURAL AND PHYSIOLOGIC CHANGES IN THE AGING LUNG
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 40
- Probably not a substantial claim. 8
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Natural lung aging is associated with molecular and physiological changes that cause alterations in lung function, diminished pulmonary remodeling and regenerative capacity, and increased susceptibility to acute and chronic lung diseases.”
§ Aging and Lung Disease > Abstract
What the sources say
- Partly supportedcites [3] sourceExperimental — accuracy not yet measured
In “Senescence in normal aging” (page unavailable), the paper discusses reduced tissue-repair capacity and suggests that extracellular-matrix changes could reduce lung elasticity. “Impact of senescence on human health” (page unavailable) also describes aging tissue as less functional and more vulnerable to stress. It does not establish the claimed lung-specific loss of remodeling and regeneration or increased susceptibility to acute and chronic lung diseases; it explicitly notes that a causal link between senescence and natural aging remains unproven. (LLM, conf=0.86)
- Not checked yetcites [4] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“There is an age-associated reduction in naïve T cell numbers that corresponds with increased memory T cell numbers (131).”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG > CD4+ and CD8+ lymphocytes.
What the sources say
- Supportedcites [131] source
The ‘Defects in T Cells with Aging’ section states that a notable age-related change is a decline in the number of naïve T cells in favor of cells with a memory phenotype. This directly supports the cited sentence. (LLM, conf=0.94)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
None of the sources cited for this claim have been checked yet.
In the paper
“Longitudinal studies have illustrated that pulmonary function impairment is a predictor for morbidity and mortality and may promote the development of multiple disease processes (1, 2).”
§ Aging and Lung Disease > INTRODUCTION
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Senescent cells display a genetic and morphologic phenotype that is distinct from growth-competent cells and can have a detrimental impact on neighboring cells, structural components, and composition of the extracellular matrix (ECM) (3).”
§ Aging and Lung Disease > INTRODUCTION
What the sources say
- Not checked yetcites [3] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Elastic recoil of the lungs, due to a reduction in the surface tension forces caused by increased individual diameters of alveoli, is reduced with aging and gives rise to an increase in end-expiratory lung volume (7, 8).”
§ Aging and Lung Disease > STRUCTURAL AND PHYSIOLOGIC CHANGES IN THE AGING LUNG
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In healthy aging, common cellular stresses can yield primary senescent cells that diminish tissue-repair capacity due to cell cycle arrest in progenitor cells and increase production of proinflammatory and matrix-degrading molecules (3, 4).”
§ Aging and Lung Disease > INTRODUCTION
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“As a result, some airways may be narrowed or closed during normal tidal breathing in older individuals, thereby increasing the functional residual capacity and reducing the expiratory airflow from the lungs (12, 13).”
§ Aging and Lung Disease > STRUCTURAL AND PHYSIOLOGIC CHANGES IN THE AGING LUNG
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“While cellular senescence in resident cells in response to intrinsic and extrinsic factors may lead to both age- and disease-related changes in the lung, it is important to note that senescence in circulating immune cells can also impact lung aging and disease progression.”
§ Aging and Lung Disease > INTRODUCTION
plainconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“As a person ages, there is a decrease in resting arterial oxygen tension, which gives rise to diminished gas exchange in the lungs (7, 12, 22).”
§ Aging and Lung Disease > STRUCTURAL AND PHYSIOLOGIC CHANGES IN THE AGING LUNG
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Many of these changes, as highlighted in Figure 1, give rise to decreased lung function, altered pulmonary remodeling, diminished regeneration, and enhanced susceptibility to pulmonary disease (7, 10).”
§ Aging and Lung Disease > CELLULAR CHANGES IN THE AGED LUNG
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“In addition, aged DCs maintain the ability to upregulate chemokines and chemokine receptors but exhibit decreased migratory capacity in response to stimuli (114).”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG > Dendritic cells.
What the sources say
- Not checked yetcites [114] source
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Changes in fibroblast function and ECM composition can increase susceptibility of the aged lung to injury and disease progression.”
§ Aging and Lung Disease > CELLULAR CHANGES IN THE AGED LUNG > Fibroblasts and the extracellular matrix.
plainconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Poor prognosis and recovery in pulmonary inflammatory diseases have been attributed to age-related changes in innate and adaptive immune responses in the lung.”
- Also stated in: § CONCLUSIONS AND FUTURE DIRECTIONS · plain
“Poor prognosis and recovery in pulmonary inflammatory diseases have been attributed to age-related changes in innate and adaptive immune responses in the lung.”
- Also stated in: § CONCLUSIONS AND FUTURE DIRECTIONS · plain
“and recovery in pulmonary inflammatory diseases have been attributed to age-related changes in innate and adaptive immune responses in the lung.”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG
plaindirect- Asserted: passes — The authors put it forward as true.
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- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
- Also stated in: § CONCLUSIONS AND FUTURE DIRECTIONS · plain
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Immunosenescence, or aging of the immune system, results from an imbalance between inflammatory and anti-inflammatory mechanisms.”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“An age-associated alteration in pathogen-mediated destruction by NETs further contributes to impaired bacterial clearance and may underlie increase susceptibility of older persons to infection (122).”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG > Neutrophils.
What the sources say
- Not checked yetcites [122] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Chronic antigen stimulation throughout a lifetime as well as oxidative stress and the production of oxygen free radicals augment production of proinflammatory cytokines.”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Age-associated changes in immune cell function can promote increased susceptibility of older persons to the development and progression of lung disorders.”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG > Innate Immunity.
plainconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Although the number of circulating neutrophils is preserved in older persons, a decrease in CD16 expression results in augmented superoxide generation and impaired neutrophil-mediated phagocytosis (120, 121).”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG > Neutrophils.
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“There is an age-associated decline in phagocytic capacity in alveolar and pulmonary macrophages, which results in impaired and/or delayed pathogen clearance from the lung (106–108).”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG > Alveolar macrophages.
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“There is an age-associated reduction in the upregulation of costimulatory molecules critical for T cell priming and dysregulated cytokine production by DCs (115, 117).”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG > Dendritic cells.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In sum, the conducting airways play a pivotal role in maintaining lung homeostasis and age-associated changes in composition and function can be partly responsible for increased susceptibility of older persons to lung disorders.”
§ Aging and Lung Disease > CELLULAR CHANGES IN THE AGED LUNG > Conducting Airways
plainconditional- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Decreased CD4+ and CD8+ T cell responses in the elderly can impair immunity to influenza vaccination and cytotoxicity against the influenza virus, respectively (132, 133).”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG > CD4+ and CD8+ lymphocytes.
plainconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“While the functional ability to produce antibody remains intact, age-associated changes in antibody specificity and antigen affinity result in a diminished ability to mount robust antibody responses in older persons (135).”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG > B lymphocytes.
What the sources say
- Not checked yetcites [135] source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Further, memory T cell responses, T cell receptor repertoire diversity, T helper cell differentiation, and T helper cell activity diminish with age (131, 132).”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG > CD4+ and CD8+ lymphocytes.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, chronic antigen stimulation throughout a lifetime as well as oxidative stress and the production of oxygen free radicals impair adaptive immune responses in the lung.”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG > B lymphocytes.
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Specifically, there is an age-associated delay in neutrophil recruitment or, in some instances, increased neutrophil accumulation due to a failure to disperse at the site of infection (123).”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG > Neutrophils.
What the sources say
- Not checked yetcites [123] Nomellini V, 2012, Aging Dis
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Rests on an assumption: Findings from experimental animal models of infection or injury are representative of human aging and can support conclusions about older persons.
None of the sources cited for this claim have been checked yet.
In the paper
“Increasing numbers of recruited neutrophils can promote the development of edema, enhanced disease severity, prolonged inflammation, and pulmonary tissue damage (125, 126).”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG > Neutrophils.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In healthy older adults, there is an increased proportion of neutrophils and a lower percentage of macrophages present in bronchoalveolar lavage (BAL) fluids (121).”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG > Neutrophils.
What the sources say
- Not checked yetcites [121] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Specifically, the ratio of CD4+ to CD8+ lymphocytes in the BAL fluid has been shown to increase with age, suggesting a decrease in the number of naïve T cells available that can be converted to memory cells against a novel antigen (131, 132).”
§ Aging and Lung Disease > IMMUNITY AND INFLAMMATION IN THE AGED LUNG > CD4+ and CD8+ lymphocytes.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Glycolytic reprogramming has been shown to play an important role in the pathogenesis of lung fibrosis, with higher glycolytic activity detected in fibrotic areas (143).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Aging and Interstitial Lung Disease
What the sources say
- Not checked yetcites [143] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“COPD is also associated with abnormalities in ciliary function and decreased mucociliary clearance, which can lead to increased incidence of recurrent infections, bronchiectasis, and airway obstruction (19, 63, 64, 86, 140).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Chronic Obstructive Pulmonary Disease
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together, although allergies and asthma can affect all age groups, asthma in the elderly in regards to inflammation and clinical manifestation is different from asthma in younger patients.”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Age-Associated Lung Function Decline with Asthma
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“While mortality from asthma has declined in the majority of age groups, the number of deaths in elderly has remained constant (140).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Age-Associated Lung Function Decline with Asthma
What the sources say
- Not checked yetcites [140] Incalzi RA, 1989, Compr. Gerontol. A
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Interestingly, many of the anatomical and physiological changes seen in COPD, such as airspace dilation resulting from loss of supporting tissue without alveolar wall destruction, have also been described in the similarly aged lungs of nonsmokers, further illustrating that the process of aging is a contributing factor for disease progression (Figure 2) (7, 10, 16).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Chronic Obstructive Pulmonary Disease
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Increased and prolonged neutrophil recruitment in the COPD lung can have devastating effects on lung parenchyma and can enhance disease severity, prolong inflammation, and cause further tissue damage (107, 125, 126).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Chronic Obstructive Pulmonary Disease
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Specifically, macrophages, which can produce multiple proinflammatory cytokines and secrete MMPs, are the most abundant cell type in the BAL fluid of COPD patients, and increased numbers correlate with disease severity (85, 86, 104).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Chronic Obstructive Pulmonary Disease
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Despite an age-associated decline in IgE production, a relationship still exists between heightened IgE levels and the development of asthma in the elderly (140).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Age-Associated Lung Function Decline with Asthma
What the sources say
- Not checked yetcites [140] Incalzi RA, 1989, Compr. Gerontol. A
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“IPF is a process that is characterized by epithelial cell injury, fibroblast expansion, augmented ECM remodeling, and lung architecture destruction (87, 141).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Aging and Interstitial Lung Disease
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Acute exacerbations of COPD (AECOPD) are common in patients with severe and very severe COPD and are characterized by increased dyspnea, purulence, and augmented sputum volume (86, 137).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Chronic Obstructive Pulmonary Disease
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Specifically, aged fibroblasts have augmented glucose utilization and increased resistance to apoptosis, which may underlie increased susceptibility of the aged lung to fibrogenesis (144).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Aging and Interstitial Lung Disease
What the sources say
- Not checked yetcites [144] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“However, when compared to aging lungs, there is a significant increase in collagen, fibronectin, and laminin, with more disorganized collagen fibers present in COPD lungs (139).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Chronic Obstructive Pulmonary Disease
What the sources say
- Not checked yetcites [139] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Further, elderly patients exhibit reduced tolerance to systemic inflammation, with increased mortality when compared with younger septic individuals (146–148).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Sepsis and Acute Respiratory Distress Syndrome in the Elderly
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Patients with severe sepsis and septic shock often require mechanical ventilation, which in the elderly is independently associated with increased mortality (146, 147).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Sepsis and Acute Respiratory Distress Syndrome in the Elderly
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“ARDS, the most severe form of acute lung injury, is a severe respiratory illness, with older patients having a higher risk of ARDS development (146).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Sepsis and Acute Respiratory Distress Syndrome in the Elderly
What the sources say
- Not checked yetcites [146] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Normal lung aging is associated with multiple structural and functional changes in the respiratory tract, with many of these changes contributing to decreased lung function, altered pulmonary remodeling, diminished regeneration, and enhanced susceptibility to pulmonary disease.”
§ Aging and Lung Disease > CONCLUSIONS AND FUTURE DIRECTIONS
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Upregulation of epithelial cell surface receptors in response to chronic inflammation increases bacterial adhesion and accumulation in the aged lung and correlates with susceptibility to pneumonia (62, 97).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Pneumonia
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Mortality rates associated with severe sepsis also increase with age, with a 50–60% mortality rate in elderly patients (146).”
§ Aging and Lung Disease > THE IMPACT OF AGING ON LUNG DISEASE > Sepsis and Acute Respiratory Distress Syndrome in the Elderly
What the sources say
- Not checked yetcites [146] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
Findings from experimental animal models of infection or injury are representative of human aging and can support conclusions about older persons.
“Experimental models of infection or injury have demonstrated that neutrophil chemotaxis is dysregulated (123).”
“In experimental models, DC migration into the aged lung during influenza infection is reduced (115).”
The paper relies on this without support.
Findings from experimental murine studies of B cell development are representative of human B cell aging.
“Specifically, experimental murine studies have demonstrated a decline in the number pro-B, pre-B, and immature B cell subsets present in older animals (135).”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Notably, immune cell disorganization associated with aging may contribute to the heightened severity of COVID-19 and chronic obstructive pulmonary disease (COPD) in the elderly.169,177”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [169]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The aging process brings about notable transformations in the structure and function of the lungs, including a decline in mucociliary clearance and heightened vulnerability to pulmonary infections.168,169”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [169]
The cited source says what the claim attributes to it.
In the citing paper
“These alterations contribute to the onset and progression of various lung diseases like idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD).169”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [169]
Citations
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Metadata
- Authors
- Cho, S. J., & Stout-Delgado, H. W.
- Affiliations
- Weill Cornell Medicine (US)
- Venue
- Annual Review of Physiology
- Publisher
- Annual Reviews
- Published
- 2020-02-10
- Volume
- 82
- Issue
- 1
- Pages
- 433-459
- ISSN
- 0066-4278 (ISSN-L)
- 1545-1585
- PMC
- PMC7998901
- OpenAlex
- W2984453596
- Semantic Scholar
- 5c4fdd1b28fbf29457689f29b4a53546ad992c99
- Cited by
- 458
- References
- 146
- Citations by year
- 2026: 50 · 2025: 113 · 2024: 109 · 2023: 94 · 2022: 53 · 2021: 21 · 2020: 14
- FWCI
- 3.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annual Review of Physiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (R01AG056699, R01AG052530)
- National Heart, Lung, and Blood Institute (K08HL138285)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Health Sciences › Medicine › Surgery › Transplantation: Methods and Outcomes
- Keywords
- lung aging, chronic obstructive pulmonary disease, interstitial pulmonary fibrosis, lung remodeling, lung infection susceptibility, immunosenescence, lung function decline
- MeSH terms
- Aged, Aging, Humans, Lung, Lung Diseases, Middle Aged, Cellular Senescence
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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