Is TP53INP2 a critical regulator of muscle mass?

Current Opinion in Clinical Nutrition and Metabolic Care
David Sala, Antonio Zorzano

Abstract

The main aim of this review is to summarize current knowledge of tumor protein p53-inducible nuclear protein 2 (TP53INP2) function and its role in skeletal muscle proteostasis. Autophagy is directly involved in the regulation of skeletal muscle mass. Thus, excessive autophagy is associated with several diseases that cause muscle wasting, and it promotes the loss of muscle protein. Furthermore, compromised autophagy also leads to muscle atrophy. In this regard, TP53INP2 activates autophagy in skeletal muscle, thus causing a reduction in muscle mass. Moreover, TP53INP2 gain of function enhances muscle wasting in a highly catabolic context such as in streptozotocin-induced diabetes. However, TP53INP2 is naturally repressed in human insulin resistance and in murine models of diabetes. These observations suggest that TP53INP2 repression would reduce muscle atrophy under conditions that favor protein loss in skeletal muscle. To date, there is no effective treatment for muscle wasting. Thus, the identification of new putative pharmacological targets to effectively treat this devastating condition is crucial. Given current knowledge about the role of TP53INP2 in skeletal muscle, this protein may be an optimal candidate to target for th...Continue Reading

References

Mar 17, 2007·Diabetes Care·Seok Won ParkUNKNOWN Health, Aging, and Body Composition Study
Nov 22, 2007·PloS One·Bernhard G BaumgartnerAntonio Zorzano
Dec 17, 2009·EMBO Reports·Caroline MauvezinAntonio Zorzano
Oct 5, 2010·Current Biology : CB·Víctor A FrancisAurelio A Teleman
Oct 26, 2011·Molecular and Cellular Biology·Sebastian AlersBjörn Stork
Apr 6, 2012·Journal of Cachexia, Sarcopenia and Muscle·Kunihiro Sakuma, Akihiko Yamaguchi
Jul 4, 2012·FEBS Letters·Caroline MauvezinAntonio Zorzano
Aug 17, 2012·American Journal of Physiology. Endocrinology and Metabolism·Jia QiuSrinivasan Dasarathy
Feb 12, 2013·The American Journal of Pathology·Fabio PennaPaola Costelli
Feb 15, 2013·The New England Journal of Medicine·Augustine M K ChoiBeth Levine
Mar 30, 2013·Journal of Cachexia, Sarcopenia and Muscle·Jerneja FarkasMitja Lainscak
Apr 4, 2013·The Journal of Clinical Investigation·Jibin ZhouThomas Force
May 15, 2013·The International Journal of Biochemistry & Cell Biology·Marco Sandri
Jun 12, 2013·Journal of Cachexia, Sarcopenia and Muscle·Kamyar Kalantar-ZadehCsaba P Kovesdy
Aug 21, 2013·The FEBS Journal·Fergal O FarrellHarald Stenmark
Sep 28, 2013·Essays in Biochemistry·Moran Rawet Slobodkin, Zvulun Elazar
Mar 26, 2014·Nature Reviews. Endocrinology·Martin PicardBruce S McEwen
Apr 10, 2014·The Journal of Clinical Investigation·David SalaAntonio Zorzano
May 31, 2014·Nature Cell Biology·Alexandra StolzIvan Dikic
Jun 8, 2014·Current Opinion in Genetics & Development·Jaime L Schneider, Ana Maria Cuervo
Jul 2, 2014·Nature Reviews. Nephrology·Xiaonan H Wang, William E Mitch
Sep 11, 2014·International Journal of Cardiology·Sandra PalusJochen Springer

❮ Previous
Next ❯

Related Concepts

Related Feeds

Cancer Metabolism

In order for cancer cells to maintain rapid, uncontrolled cell proliferation, they must acquire a source of energy. Cancer cells acquire metabolic energy from their surrounding environment and utilize the host cell nutrients to do so. Here is the latest research on cancer metabolism.

Cachexia & Brown Fat

Cachexia is a condition associated with progressive weight loss due to severe illness. In cancer patients, it is proposed to occur as a result of tumor-induced energy wasting. Several proteins have been implicated in browning and depletion of white adipose tissue. Here is the latest research on cachexia and brown fat.

Cardiac Cachexia

Cardiac cachexia is a syndrome associated with the progressive loss of muscle and fat mass. It most commonly affects patients with heart failure and can significantly decrease the quality of life and survival in these patients. Here is the latest research on cardiac cachexia.

Autophagy & Model Organisms

Autophagy is a cellular process that allows degradation by the lysosome of cytoplasmic components such as proteins or organelles. Here is the latest research on autophagy & model organisms

Autophagy & Disease

Autophagy is an important cellular process for normal physiology and both elevated and decreased levels of autophagy are associated with disease. Here is the latest research.

Autophagy Networks

Autophagy is a lysosomal pathway that involves degradation of proteins and functions in normal growth and pathological conditions, through a series of complex networks. The catabolic process involves delivery of proteins and organelles to the lysosome. Here is the latest research on autophagy networks.

Related Papers

Nestlé Nutrition Workshop Series. Clinical & Performance Programme
Simon P Allison, Amparo Martinez-Riquelme
© 2021 Meta ULC. All rights reserved