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Table 2 Summary of studies using Apoe−/− mice conducted by PMI

From: The Apoe−/− mouse model: a suitable model to study cardiovascular and respiratory diseases in the context of cigarette smoke exposure and harm reduction

Disease, mechanism

References

Biological matrix

Endpoint

Effect of CS exposure

Effect of cessation

CVD

[116]

Aorta

Lipidomics

ND

CVD

[117]

Aorta

Lipidomics

↓→

CVD

[19]

Aorta

Lipidomics

↓→

CVD

[42]

Carotid artery

Thrombosis

ND

CVD

[42]

Carotid artery

Endothelial injury

ND

CVD

[116]

Liver

Lipidomics

↑→

ND

CVD

[118]

Liver

Lipidomics

↓↑

CVD

[114]

Liver

Lipidomics

CVD

[118]

Liver

Transcriptomics

CVD

[114]

Liver

Transcriptomics

CVD

[114]

Liver

Proteomics

CVD

[116]

Plasma

Lipidomics

ND

CVD

[117]

Plasma

Lipidomics

↑→

↓→

CVD

[19]

Plasma

Lipidomics

COPD

[113]

Lung

Lipidomics

COPD

[113]

Lung

Transcriptomics

COPD

[113]

Lung

Proteomics

Atherosclerosis

[116]

Aorta

Plaque size

ND

Atherosclerosis

[117]

Aorta

Plaque size

Atherosclerosis

[19]

Aorta

Plaque size

Atherosclerosis

[118]

Aorta

Plaque size

ND

Atherosclerosis

[29]

Aorta

Plaque size

ND

Atherosclerosis

[27]

BA

Plaque size

↑→

ND

Atherosclerosis

[27]

Aortic arch

Plaque size

↑→

ND

Exposure markers

[18]

Blood

COHb

Exposure markers

[18]

Urine

Nicotine metabolites

Exposure marker

[117]

Blood

COHb

Exposure marker

[118]

Blood

COHb

Exposure marker

[117]

Urine

Nicotine metabolites

Exposure markers

[19]

Blood

COHb

Exposure markers

[19]

Urine

Nicotine metabolites

Inflammation

[18]

Lung

BALF

Inflammation

[18]

NRE

Histopathology

Inflammation

[18]

Lung

Transcriptomics

↑↓

↓↑

Inflammation

[116]

Liver

Transcriptomics

ND

Inflammation

[124]

Lung

BALF

↑→

Inflammation

[29]

Aorta

Transcriptomics

ND

Inflammation

[127]

Lung

Transcriptomics

↑↓

ND

Inflammation

[127]

Lung

BALF

ND

Inflammation

[127]

Respiratory

Histopathology

ND

Inflammation

[127]

Respiratory

Network model

ND

Inflammation

[113]

Lung

Lipidomics

Inflammation

[19]

Urine

Inflammatory biomarker

Inflammation

[19]

Lung

BALF

Inflammation

[19]

NRE

Histopathology

Inflammation

[19]

Lung

Histopathology

COPD—emphysema

[18]

Lung

Lung morphometry

COPD—emphysema

[19]

Lung

Lung function

COPD—emphysema

[19]

Lung

Lung morphometry

Inflammation/cell cycle/necroptosis

[19]

Lung

Network model

Inflammation/cell cycle/necroptosis

[19]

Lung

Transcriptomics

Inflammation/cell cycle/necroptosis

[19]

Lung

Proteomics

Inflammation/cell cycle/necroptosis

[124]

Lung

Network model

Inflammation/cell cycle/necroptosis

[124]

Lung

Transcriptomics

Oxidative stress

[18]

Lung

BALF

Oxidative stress

[18]

NRE

Transcriptomics

↑↓

↓↑

Oxidative stress

[114]

Liver

Transcriptomics

Oxidative stress

[114]

Liver

Proteomics

  1. Arrows indicate increase (upwards), decrease (downwards), no change (to the right), trend to increase (north east), and trend to decrease (south east). Arrows for the cigarette smoke (CS) effect indicate changes compared with unexposed mice, and arrows for the cessation effect indicate differences compared with continued CS exposure
  2. COHb carboxyhemoglobin; BALF bronchoalveolar lavage fluid; CVD cardiovascular disease; NRE nasal respiratory epithelium; COPD chronic obstructive pulmonary disease; BA brachiocephalic artery; ND not done