The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4

By Chanhee Kang, Qikai Xu, Timothy D. Martin, Mamie Z. Li, M. Demaria, Liviu Aron, Tao Lu, B. Yankner, J. Campisi, Stephen J. Elledge. Science, 2015

870 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/1c8d59d11fcdf222bbe3773e00513f264d268be0

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. L. Galluzzi
2. Guido Kroemer
3. Frank Madeo
4. C. López‐Otín
5. Jesús Gil
6. Domhnall McHugh
7. M. Demaria
8. Beth Levine

In Molecular Biology

1. Guido Kroemer
2. L. Galluzzi
3. Frank Madeo
4. Jesús Gil
5. C. López‐Otín
6. T. von Zglinicki
7. Satomi Miwa
8. A. Alimonti

In Physiology

1. L. Galluzzi
2. Guido Kroemer
3. Jesús Gil
4. C. López‐Otín
5. T. von Zglinicki
6. A. Alimonti
7. J. Kohli
8. E. Zagato

Citations in the corpus

• Innate immune sensing of cytosolic chromatin fragments through cGAS promotes senescence (2017, neutral): “On a molecular level, several transcription factors have been implicated in the up-regulation of SASP-genes including NF-κ B, C/EBP-β , p38 MAPK and GATA4 12, 13, 14, 15, 16.”
• Mitochondrial dysfunction in cell senescence and aging (2022, background): “Furthermore, inhibition of selective autophagy for the transcription factor GATA4 was associated with induction of senescence (77).”
• Mechanisms and functions of cellular senescence. (2018, neutral): “However, the regulation of the SASP by autophagy is complex, as GATA4 controls the SASP by inhibiting autophagy (94).”
• Senescence and aging: Causes, consequences, and therapeutic avenues (2018, background): “DNA damage (Rodier et al., 2009), p38α MAPK (Freund et al., 2011), mTOR (Herranz et al., 2015; Laberge et al., 2015), mixed lineage leukemia 1 (Capell et al., 2016), and GATA4 (Kang et al., 2015) are also able to regulate Senescence and aging • mcHugh and Gil 69 the SASP.”
• Metabolic Control of Longevity. (2016, background): “The so-called ‘‘senescence-associated secretory phenotype’’ (SASP), which is a pathognomonic shift in protein secretion, stems from the dissociation of the transcription factor GATA4 and the autophagic adaptor p62 (Kang et al., 2015).”
• The senescence-associated secretory phenotype and its physiological and pathological implications (2024, neutral): “Finally, other DDR factors, including ATM–CHK2, ATR and GATA4, also promote pro-inflammatory SASP 69,70,77 (Fig.”
• Mechanisms of Vascular Aging (2018, background): “age response pathway, and GATA4 (transcription factor GATA-4).(82,83) There is growing evidence that the presence”
• Hallmarks of Cellular Senescence. (2018, neutral): “Additional transcription factors involved in the regulation of SASP genes are GATA4 and C/EBPb [57,58].”
• Senescence and the SASP: many therapeutic avenues (2020, background): “Increased stabilization of the transcription factor GATAbinding protein 4 (GATA4) connects the DDR with NFκB activation to induce the SASP (Kang et al. 2015).”
• Cellular Senescence: Aging, Cancer, and Injury. (2019, background): “The transcription factor GATA4, acting upstream of NF- B, is also required for senescence establishment and SASP induction (177).”