Mycobacterium tuberculosis-Driven Targeted Recalibration of Macrophage Lipid Homeostasis Promotes the Foamy Phenotype
TLDR
It is found that Mtb induces the foamy phenotype via targeted manipulation of host cellular metabolism to divert the glycolytic pathway toward ketone body synthesis, and pharmacological targeting of pathways mediating this host-pathogen metabolic crosstalk provides a potential strategy for developing tuberculosis chemotherapy.About:
This article is published in Cell Host & Microbe.The article was published on 2012-11-15 and is currently open access. It has received 228 citations till now.read more
Citations
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Macrophage defense mechanisms against intracellular bacteria.
Günter Weiss,Ulrich E. Schaible +1 more
TL;DR: Gaining more insights and knowledge into this complex network of host‐pathogen interaction will identify novel target sites of intervention to successfully clear infection at a time of rapidly emerging multi‐resistance of M. tuberculosis against conventional antibiotics.
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Dietary gut microbial metabolites, short-chain fatty acids, and host metabolic regulation.
TL;DR: The roles of gut microbial SCFAs in the host energy regulation are summarized and an overview of the current understanding of its physiological functions is presented.
Journal ArticleDOI
Are reactive oxygen species always detrimental to pathogens
TL;DR: This study reviews the classic infections that are controlled by ROS and the cases in which ROS appear as promoters of infection, challenging the paradigm, and discusses the possible mechanisms by which ROS could promote particular infections.
Journal ArticleDOI
Free Fatty Acid Receptors in Health and Disease.
TL;DR: Recent reports on the key physiological functions of the FFAR-mediated signaling transduction pathways in the regulation of metabolism and immune responses are discussed and future research opportunities for developing therapeutics for metabolic and immune disorders are revealed.
Journal ArticleDOI
PGC1α drives NAD biosynthesis linking oxidative metabolism to renal protection
Mei T. Tran,Zsuzsanna K. Zsengellér,Anders H. Berg,Eliyahu V. Khankin,Manoj Bhasin,Wondong Kim,Clary B. Clish,Isaac E. Stillman,S. Ananth Karumanchi,S. Ananth Karumanchi,Eugene P. Rhee,Eugene P. Rhee,Samir M. Parikh +12 more
TL;DR: It is shown that the mitochondrial biogenesis regulator, PGC1α, is a pivotal determinant of renal recovery from injury by regulating nicotinamide adenine dinucleotide (NAD) biosynthesis, and NAM treatment reverses established ischaemic AKI and also prevented AKI in an unrelated toxic model.
References
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