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Cell Commun Signal. 2016 Jan 12;14:3. doi: 10.1186/s12964-016-0126-1.

GPR91: expanding the frontiers of Krebs cycle intermediates.

Author information

1
Department of Physiology and Biophysics, Federal University of Minas Gerais, Av. Antonio Carlos 6627, Belo Horizonte, MG, CEP: 31270-901, Brazil. hp.matheus@gmail.com.
2
Centro Universitário Estácio de Sá, Belo Horizonte, MG, Brazil. carlajeane33@hotmail.com.
3
Department of Physiology and Biophysics, Federal University of Minas Gerais, Av. Antonio Carlos 6627, Belo Horizonte, MG, CEP: 31270-901, Brazil. joaoantoniodarochafranco@hotmail.com.
4
Department of Physiology and Biophysics, Federal University of Minas Gerais, Av. Antonio Carlos 6627, Belo Horizonte, MG, CEP: 31270-901, Brazil. r.n.gingold@gmail.com.
5
Department of Physiology and Biophysics, Federal University of Minas Gerais, Av. Antonio Carlos 6627, Belo Horizonte, MG, CEP: 31270-901, Brazil. leitemd@ufmg.br.

Abstract

Since it was discovered, the citric acid cycle has been known to be central to cell metabolism and energy homeostasis. Mainly found in the mitochondrial matrix, some of the intermediates of the Krebs cycle are also present in the blood stream. Currently, there are several reports that indicate functional roles for Krebs intermediates out of its cycle. Succinate, for instance, acts as an extracellular ligand by binding to a G-protein coupled receptor, known as GPR91, expressed in kidney, liver, heart, retinal cells and possibly many other tissues, leading to a wide array of physiological and pathological effects. Through GPR91, succinate is involved in functions such as regulation of blood pressure, inhibition of lipolysis in white adipose tissue, development of retinal vascularization, cardiac hypertrophy and activation of stellate hepatic cells by ischemic hepatocytes. Along the current review, these new effects of succinate through GPR91 will be explored and discussed.

PMID:
26759054
PMCID:
PMC4709936
DOI:
10.1186/s12964-016-0126-1
[Indexed for MEDLINE]
Free PMC Article

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