PMID- 31681260
OWN - NLM
STAT- MEDLINE
DCOM- 20201103
LR  - 20230503
IS  - 1664-3224 (Electronic)
IS  - 1664-3224 (Linking)
VI  - 10
DP  - 2019
TI  - Metabolic Programming of Macrophages: Implications in the Pathogenesis of 
      Granulomatous Disease.
PG  - 2265
LID - 10.3389/fimmu.2019.02265 [doi]
LID - 2265
AB  - Metabolic reprogramming is rapidly gaining appreciation in the etiology of immune 
      cell dysfunction in a variety of diseases. Tuberculosis, schistosomiasis, and 
      sarcoidosis represent an important class of diseases characterized by the 
      formation of granulomas, where macrophages are causatively implicated in disease 
      pathogenesis. Recent studies support the incidence of macrophage metabolic 
      reprogramming in granulomas of both infectious and non-infectious origin. These 
      publications identify the mechanistic target of rapamycin (mTOR), as well as the 
      major regulators of lipid metabolism and cellular energy balance, peroxisome 
      proliferator receptor gamma (PPAR-gamma) and adenosine monophosphate-activated 
      protein kinase (AMPK), respectively, as key players in the pathological 
      progression of granulomas. In this review, we present a comprehensive breakdown 
      of emerging research on the link between macrophage cell metabolism and 
      granulomas of different etiology, and how parallels can be drawn between 
      different forms of granulomatous disease. In particular, we discuss the role of 
      PPAR-gamma signaling and lipid metabolism, which are currently the best-represented 
      metabolic pathways in this context, and we highlight dysregulated lipid 
      metabolism as a common denominator in granulomatous disease progression. This 
      review therefore aims to highlight metabolic mechanisms of granuloma immune cell 
      fate and open up research questions for the identification of potential 
      therapeutic targets in the future.
CI  - Copyright (c) 2019 Wilson, Mayr and Weichhart.
FAU - Wilson, Jayne Louise
AU  - Wilson JL
AD  - Center for Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical 
      University of Vienna, Vienna, Austria.
FAU - Mayr, Hannah Katharina
AU  - Mayr HK
AD  - Center for Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical 
      University of Vienna, Vienna, Austria.
FAU - Weichhart, Thomas
AU  - Weichhart T
AD  - Center for Pathobiochemistry and Genetics, Institute of Medical Genetics, Medical 
      University of Vienna, Vienna, Austria.
LA  - eng
GR  - P 27701/FWF_/Austrian Science Fund FWF/Austria
GR  - P 30857/FWF_/Austrian Science Fund FWF/Austria
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20191004
PL  - Switzerland
TA  - Front Immunol
JT  - Frontiers in immunology
JID - 101560960
RN  - 0 (PPAR gamma)
RN  - EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
SB  - IM
MH  - AMP-Activated Protein Kinases/physiology
MH  - Cell Polarity
MH  - Citric Acid Cycle
MH  - Granuloma/*etiology
MH  - Humans
MH  - Lipid Metabolism
MH  - Macrophage Activation
MH  - Macrophages/*metabolism
MH  - Mechanistic Target of Rapamycin Complex 1/physiology
MH  - PPAR gamma/physiology
MH  - Sarcoidosis/complications/metabolism
MH  - Schistosomiasis/complications/metabolism
MH  - Signal Transduction
MH  - Tuberculosis/complications/metabolism
PMC - PMC6797840
OTO - NOTNLM
OT  - granuloma
OT  - immunometabolism
OT  - macrophage
OT  - sarcoidosis
OT  - schistosomiasis
OT  - tuberculosis
EDAT- 2019/11/05 06:00
MHDA- 2020/11/04 06:00
PMCR- 2019/01/01
CRDT- 2019/11/05 06:00
PHST- 2019/06/14 00:00 [received]
PHST- 2019/09/09 00:00 [accepted]
PHST- 2019/11/05 06:00 [entrez]
PHST- 2019/11/05 06:00 [pubmed]
PHST- 2020/11/04 06:00 [medline]
PHST- 2019/01/01 00:00 [pmc-release]
AID - 10.3389/fimmu.2019.02265 [doi]
PST - epublish
SO  - Front Immunol. 2019 Oct 4;10:2265. doi: 10.3389/fimmu.2019.02265. eCollection 
      2019.