Activation of the mTORC1/PGC-1 axis promotes mitochondrial biogenesis and induces cellular senescence in the lung epithelium Article Swipe
Ross Summer
,
Hoora Shaghaghi
,
DeLeila Schriner
,
Willy Roque
,
Dominic Sales
,
Karina Cuevas-Mora
,
Vilas Desai
,
Alok Bhushan
,
María I. Ramirez
,
Freddy Romero
·
YOU?
·
· 2019
· Open Access
·
· DOI: https://doi.org/10.1152/ajplung.00244.2018
YOU?
·
· 2019
· Open Access
·
· DOI: https://doi.org/10.1152/ajplung.00244.2018
Cellular senescence is a biological process by which cells lose their capacity to proliferate yet remain metabolically active. Although originally considered a protective mechanism to limit the formation of cancer, it is now appreciated that cellular senescence also contributes to the development of disease, including common respiratory ailments such as chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. While many factors have been linked to the development of cellular senescence, mitochondrial dysfunction has emerged as an important causative factor. In this study, we uncovered that the mitochondrial biogenesis pathway driven by the mammalian target of rapamycin/peroxisome proliferator-activated receptor-γ complex 1α/β (mTOR/PGC-1α/β) axis is markedly upregulated in senescent lung epithelial cells. Using two different models, we show that activation of this pathway is associated with other features characteristic of enhanced mitochondrial biogenesis, including elevated number of mitochondrion per cell, increased oxidative phosphorylation, and augmented mitochondrial reactive oxygen species (ROS) production. Furthermore, we found that pharmacological inhibition of the mTORC1 complex with rapamycin not only restored mitochondrial homeostasis but also reduced cellular senescence to bleomycin in lung epithelial cells. Likewise, mitochondrial-specific antioxidant therapy also effectively inhibited mTORC1 activation in these cells while concomitantly reducing mitochondrial biogenesis and cellular senescence. In summary, this study provides a mechanistic link between mitochondrial biogenesis and cellular senescence in lung epithelium and suggests that strategies aimed at blocking the mTORC1/PGC-1α/β axis or reducing ROS-induced molecular damage could be effective in the treatment of senescence-associated lung diseases.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1152/ajplung.00244.2018
- https://journals.physiology.org/doi/pdf/10.1152/ajplung.00244.2018
- OA Status
- bronze
- Cited By
- 129
- References
- 50
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W2923637858
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
-
https://openalex.org/W2923637858Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1152/ajplung.00244.2018Digital Object Identifier
- Title
-
Activation of the mTORC1/PGC-1 axis promotes mitochondrial biogenesis and induces cellular senescence in the lung epitheliumWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2019Year of publication
- Publication date
-
2019-03-20Full publication date if available
- Authors
-
Ross Summer, Hoora Shaghaghi, DeLeila Schriner, Willy Roque, Dominic Sales, Karina Cuevas-Mora, Vilas Desai, Alok Bhushan, María I. Ramirez, Freddy RomeroList of authors in order
- Landing page
-
https://doi.org/10.1152/ajplung.00244.2018Publisher landing page
- PDF URL
-
https://journals.physiology.org/doi/pdf/10.1152/ajplung.00244.2018Direct link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
bronzeOpen access status per OpenAlex
- OA URL
-
https://journals.physiology.org/doi/pdf/10.1152/ajplung.00244.2018Direct OA link when available
- Concepts
-
mTORC1, Mitochondrial biogenesis, Cell biology, Senescence, Mitochondrion, Biology, PI3K/AKT/mTOR pathway, Mitochondrial ROS, Cancer research, Signal transductionTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
129Total citation count in OpenAlex
- Citations by year (recent)
-
2025: 14, 2024: 21, 2023: 21, 2022: 31, 2021: 22Per-year citation counts (last 5 years)
- References (count)
-
50Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.features | 125 |
| abstract_inverted_index.markedly | 103 |
| abstract_inverted_index.provides | 201 |
| abstract_inverted_index.reactive | 144 |
| abstract_inverted_index.reducing | 191, 225 |
| abstract_inverted_index.restored | 163 |
| abstract_inverted_index.suggests | 215 |
| abstract_inverted_index.summary, | 198 |
| abstract_inverted_index.Likewise, | 177 |
| abstract_inverted_index.augmented | 142 |
| abstract_inverted_index.bleomycin | 172 |
| abstract_inverted_index.causative | 77 |
| abstract_inverted_index.different | 112 |
| abstract_inverted_index.diseases. | 238 |
| abstract_inverted_index.effective | 231 |
| abstract_inverted_index.fibrosis. | 57 |
| abstract_inverted_index.formation | 27 |
| abstract_inverted_index.important | 76 |
| abstract_inverted_index.including | 44, 131 |
| abstract_inverted_index.increased | 138 |
| abstract_inverted_index.inhibited | 183 |
| abstract_inverted_index.mammalian | 92 |
| abstract_inverted_index.mechanism | 23 |
| abstract_inverted_index.molecular | 227 |
| abstract_inverted_index.oxidative | 139 |
| abstract_inverted_index.pulmonary | 52, 56 |
| abstract_inverted_index.rapamycin | 160 |
| abstract_inverted_index.senescent | 106 |
| abstract_inverted_index.treatment | 234 |
| abstract_inverted_index.uncovered | 83 |
| abstract_inverted_index.activation | 117, 185 |
| abstract_inverted_index.associated | 122 |
| abstract_inverted_index.biogenesis | 87, 193, 207 |
| abstract_inverted_index.biological | 4 |
| abstract_inverted_index.considered | 20 |
| abstract_inverted_index.epithelial | 108, 175 |
| abstract_inverted_index.epithelium | 213 |
| abstract_inverted_index.idiopathic | 55 |
| abstract_inverted_index.inhibition | 154 |
| abstract_inverted_index.originally | 19 |
| abstract_inverted_index.protective | 22 |
| abstract_inverted_index.senescence | 1, 36, 170, 210 |
| abstract_inverted_index.strategies | 217 |
| abstract_inverted_index.ROS-induced | 226 |
| abstract_inverted_index.antioxidant | 179 |
| abstract_inverted_index.appreciated | 33 |
| abstract_inverted_index.biogenesis, | 130 |
| abstract_inverted_index.contributes | 38 |
| abstract_inverted_index.development | 41, 66 |
| abstract_inverted_index.dysfunction | 71 |
| abstract_inverted_index.effectively | 182 |
| abstract_inverted_index.homeostasis | 165 |
| abstract_inverted_index.mechanistic | 203 |
| abstract_inverted_index.obstructive | 51 |
| abstract_inverted_index.production. | 148 |
| abstract_inverted_index.proliferate | 13 |
| abstract_inverted_index.receptor-γ | 97 |
| abstract_inverted_index.respiratory | 46 |
| abstract_inverted_index.senescence, | 69 |
| abstract_inverted_index.senescence. | 196 |
| abstract_inverted_index.upregulated | 104 |
| abstract_inverted_index.Furthermore, | 149 |
| abstract_inverted_index.concomitantly | 190 |
| abstract_inverted_index.metabolically | 16 |
| abstract_inverted_index.mitochondrial | 70, 86, 129, 143, 164, 192, 206 |
| abstract_inverted_index.mitochondrion | 135 |
| abstract_inverted_index.characteristic | 126 |
| abstract_inverted_index.pharmacological | 153 |
| abstract_inverted_index.phosphorylation, | 140 |
| abstract_inverted_index.(mTOR/PGC-1α/β) | 100 |
| abstract_inverted_index.mTORC1/PGC-1α/β | 222 |
| abstract_inverted_index.rapamycin/peroxisome | 95 |
| abstract_inverted_index.senescence-associated | 236 |
| abstract_inverted_index.mitochondrial-specific | 178 |
| abstract_inverted_index.proliferator-activated | 96 |
| cited_by_percentile_year.max | 100 |
| cited_by_percentile_year.min | 94 |
| corresponding_author_ids | https://openalex.org/A5071321963 |
| countries_distinct_count | 1 |
| institutions_distinct_count | 10 |
| corresponding_institution_ids | https://openalex.org/I149251103 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.7699999809265137 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.98611237 |
| citation_normalized_percentile.is_in_top_1_percent | True |
| citation_normalized_percentile.is_in_top_10_percent | True |