A crucial role for adipose tissue p53 in the regulation of insulin resistance

By T. Minamino, Masayuki Orimo, I. Shimizu, T. Kunieda, Masataka Yokoyama, Takashi K. Ito, Aika Nojima, A. Nabetani, Y. Oike, H. Matsubara and 2 more. Nature Medicine, 2009

864 citations recorded by the source corpus.

Subfields: Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/6994a18e27534037c898386d589f9e99c75f8c74

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. P. Scherer
2. J. Campisi
3. M. Demaria
4. Haiming Cao
5. M. Blüher

In Physiology

1. J. Kirkland
2. T. Tchkonia
3. M. Demaria
4. J. Campisi
5. J. V. van Deursen
6. Yi Zhu
7. A. Alimonti
8. J. Kohli

Citations in the corpus

• The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis. (2017, positive): “The prevention of cellular senescence through inhibition of the major senescence regulator p53 attenuates metabolic abnormalities (102, 103).”
• Cellular Senescence: Aging, Cancer, and Injury. (2019, background): “Excessive caloric intake in mice induces senescence in adipose tissue via ROS-mediated activation of p53 and p21 (230).”
• Cellular senescence and the senescent secretory phenotype: therapeutic opportunities. (2013, positive): “For example, effects of senolytics on ameliorating peripheral insulin resistance in obese subjects could be tested because massive obesity is associated with fat tissue senescent cell accumulation and elevated levels of circulating SASP-re-lated cytokines that cause insulin resistance (56, 85).”
• Mechanisms and functions of cellular senescence. (2018, neutral): “However, terminally differentiated cells such as neurons, adipocytes, and hepatocytes can also undergo senescence, or at least show senescence-like features, during aging or in response to oncogenic activation or DNA damage (21, 23–25).”