A Breakdown in Metabolic Reprogramming Causes Microglia Dysfunction in Alzheimer's Disease

Cell Metabolism, Journal Year: 2019, Volume and Issue: 30(3), P. 493 - 507.e6

Published: June 27, 2019

Language: Английский

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Genome-wide enhancer maps link risk variants to disease genes

Nature, Journal Year: 2021, Volume and Issue: 593(7858), P. 238 - 243

Published: April 7, 2021

Language: Английский

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Skeletal muscle: A review of molecular structure and function, in health and disease

WIREs Systems Biology and Medicine, Journal Year: 2019, Volume and Issue: 12(1)

Published: Aug. 13, 2019

Abstract Decades of research in skeletal muscle physiology have provided multiscale insights into the structural and functional complexity this important anatomical tissue, designed to accomplish task generating contraction, force movement. Skeletal can be viewed as a biomechanical device with various interacting components including autonomic nerves for impulse transmission, vasculature efficient oxygenation, embedded regulatory metabolic machinery maintaining cellular homeostasis. The “omics” revolution has propelled new era research, allowing us discern minute details molecular cross‐talk required effective coordination between myriad function. objective review is provide systems‐level, comprehensive mapping mechanisms underlying structure function, health disease. We begin focus on tissue development (myogenesis), an emphasis satellite cells regeneration. next many muscle: neuromuscular junction, sarcomere, cytoskeleton, extracellular matrix, surrounding muscle. highlight aberrant their possible clinical or pathophysiological relevance. particularly emphasize impact environmental stressors (inflammation oxidative stress) contributing pathophysiology atrophy, hypertrophy, fibrosis. This article categorized under: Physiology > Mammalian Health Disease Developmental Biology Processes Models Systems Properties Cellular

Language: Английский

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Therapeutically exploiting STAT3 activity in cancer — using tissue repair as a road map

Nature reviews. Cancer, Journal Year: 2018, Volume and Issue: 19(2), P. 82 - 96

Published: Dec. 21, 2018

Language: Английский

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Regulation of macrophage immunometabolism in atherosclerosis

Nature Immunology, Journal Year: 2018, Volume and Issue: 19(6), P. 526 - 537

Published: May 17, 2018

Language: Английский

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Mitophagy, Mitochondrial Homeostasis, and Cell Fate

Frontiers in Cell and Developmental Biology, Journal Year: 2020, Volume and Issue: 8

Published: June 24, 2020

Mitochondria are highly plastic and dynamic organelles that have graded responses to the changing cellular, environmental developmental cues. undergo constant mitochondrial fission fusion, biogenesis mitophagy, which coordinately control morphology, quantity, quality, turnover inheritance. Mitophagy is a cellular process selectively removes aged damaged mitochondria via specific sequestration engulfment of for subsequent lysosomal degradation. It plays pivotal role reinstate homeostasis in normal physiology conditions stress. Damaged may either instigate innate immunity through overproduction ROS or release mtDNA, trigger cell death cytochrome c other apoptogenic factors when damage beyond repair. Distinct molecular machineries signaling pathways found regulate these dynamics behaviors. less clear how behaviors coordinated at levels. BCL2 family proteins interact within members outer membrane permeabilization apoptosis. They were also described as global regulators fate their interaction with distinct partners including Drp1, mitofusins, PGAM5 even LC3 involved In this review, we summarize recent findings on governing mitophagy its coordination behaviors, together determine fate.

Language: Английский

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Linking cellular stress responses to systemic homeostasis

Nature Reviews Molecular Cell Biology, Journal Year: 2018, Volume and Issue: 19(11), P. 731 - 745

Published: Oct. 10, 2018

Language: Английский

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Interplay Between NLRP3 Inflammasome and Autophagy

Frontiers in Immunology, Journal Year: 2020, Volume and Issue: 11

Published: Oct. 9, 2020

The NLRP3 inflammasome is cytosolic multi-protein complex that induces inflammation and pyroptotic cell death in response to both pathogen (PAMPs) endogenous activators (DAMPs). Recognition of PAMPs or DAMPs leads formation the complex, which results activation caspase-1, followed by cleavage release pro-inflammatory cytokines. Excessive can contribute development inflammatory diseases cancer. Autophagy vital intracellular process for recycling removal damaged proteins organelles, as well destruction pathogens. Cytosolic components are sequestered a double-membrane vesicle – autophagosome, then fuses with lysosome resulting degradation cargo. autophagy dysfunction lead hyperinflammation excessive thus acts major regulator inflammasomes. Autophagic activators, such DAMPs, cytokines reduce response. Likewise, signaling pathways regulate autophagic necessary balance between required host defense prevention detrimental inflammation. has protective role some associated inflammasome, including gouty arthritis, familial Mediterranean fever sepsis. Understanding interregulation these two essential biological processes comprehend mechanisms designing possible treatments multiple

Language: Английский

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Foundations of Immunometabolism and Implications for Metabolic Health and Disease

Immunity, Journal Year: 2017, Volume and Issue: 47(3), P. 406 - 420

Published: Sept. 1, 2017

Language: Английский

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Emerging views of mitophagy in immunity and autoimmune diseases

Autophagy, Journal Year: 2019, Volume and Issue: 16(1), P. 3 - 17

Published: April 5, 2019

Mitophagy is a vital form of autophagy for selective removal dysfunctional or redundant mitochondria. Accumulating evidence implicates elimination mitochondria as powerful means employed by to keep the immune system in check. The process mitophagy may restrict inflammatory cytokine secretion and directly regulate mitochondrial antigen presentation cell homeostasis. In this review, we describe distinctive pathways mammalian highlight recent advances relevant its function immunity. addition, further discuss direct indirect linking inflammation autoimmunity underlying pathogenesis autoimmune diseases including bowel (IBD), systemic lupus erythematosus (SLE) primary biliary cirrhosis (PBC).Abbreviations: AICD: activation induced death; AIM2: absent melanoma 2; ALPL/HOPS: alkaline phosphatase, biomineralization associated; AMA: anti-mitochondrial antibodies; AMFR: autocrine motility factor receptor; ATG: autophagy-related; BCL2L13: BCL2 like 13; BNIP3: interacting protein 3; BNIP3L/NIX: 3 like; CALCOCO2/NDP52: calcium binding coiled-coil domain CARD: caspase recruitment containing; CASP1: 1; CD: Crohn disease; CGAS: cyclic GMP-AMP synthase; CXCL1: C-X-C motif chemokine ligand DEN: diethylnitrosamine; DLAT/PDC-E2: dihydrolipoamide S-acetyltransferase; DNM1L/Drp1: dynamin 1 ESCRT: endosomal sorting complexes required transport; FKBP8: FKBP prolyl isomerase 8; FUNDC1: Fun14 containing GABARAP: GABA type A receptor-associated protein; HMGB1: high mobility group box HPIV3: human parainfluenza virus IBD: diseases; IEC: intestinal epithelial cell; IFN: interferon; IL1B/IL-1β: interleukin beta; iNK: invariant natural killer; IRGM: immunity related GTPase M; LIR: LC3-interacting region; LPS: lipopolysaccharide; LRRK2: leucine rich repeat kinase MAP1LC3/LC3: microtubule associated light chain MARCH5: membrane ring-CH-type finger 5; MAVS: antiviral signaling MDV: mitochondria-derived vesicle; MFN1: mitofusin MHC: major histocompatibility complex; MIF: macrophage migration inhibitory factor; mtAP: presentation; mtDNA: DNA; MTOR: mechanistic target rapamycin kinase; mtROS: ROS; MUL1: E3 ubiquitin ligase NBR1: NBR1 cargo NFKB/NF-ĸB: nuclear kappa B subunit; NK: NLR: NOD-like NLRC4: NLR family CARD 4; NLRP3: pyrin OGDH: oxoglutarate dehydrogenase; OMM: outer membrane; OPTN: optineurin; ox: oxidized; PARK7: Parkinsonism deglycase; PBC: cirrhosis; PEX13: peroxisomal biogenesis PHB/PHB1: prohibitin; PHB2: prohibitin PIK3C3/VPS34: phosphatidylinositol 3-kinase catalytic subunit PINK1: PTEN PLEKHM1: pleckstrin homology RUN M1; PRKN/PARK2: parkin RBR ligase; RAB: member RAS oncogene family; RHEB: Ras homolog: mTORC1 binding; RIPK2: receptor serine/threonine RLR: DDX58/RIG-I ROS: reactive oxygen species; SBD: small bile ducts; SLC2A1/GLUT1: solute carrier 2 SLE: erythematosus; SMURF1: SMAD specific SQSTM1/p62: sequestosome TAX1BP1: Tax1 TCR: T TFAM: transcription A: mitochondrial; Th17: helper 17; TLR9: toll 9; TMEM173/STING: transmembrane 173; TNF/TNF-α: tumor necrosis Ub: ubiquitin; UC: ulcerative colitis; ULK1: unc-51 activating WIPI: WD domain: phosphoinositide interacting; ZFYVE1/DFCP1: zinc FYVE-type 1.

Language: Английский

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