We are analyzing https://link.springer.com/article/10.1186/s12950-019-0212-4.

Title:
Role of autophagy in atherosclerosis: foe or friend? | Journal of Inflammation
Description:
Athrosclerosis is conceived as a chronic inflammatory status affecting cells from vascular walls. Different mechanisms and pathological features are evident at the onset of atherosclerotic changes via the engaging different cells from the vascular wall and circulatory cells. Attempts are currently focused on the detection of cell compensatory mechanisms against atherosclerotic changes to restore cell function and/or postpone severe vasculitis. Autophagy is an intracellular self-digesting process commonly protrudes exhausted organelles and injured cytoplasmic constituents via double-lipid bilayer membrane vesicles out the target cells. Recent investigations point to the critical and defensive role of autophagy in the vascular cells behavioral function such as endothelial cells and smooth muscle cells against different insults. Autophagy response and related effectors could be modulated in the favor to restore cell function and reduce pro-inflammatory status under pathological conditions. In this review, the recent findings were collected regarding the role of autophagy during atherosclerotic changes. We aimed to answer the question of how autophagy stimulation and/or inhibition could provide a promising effect on developing a sophisticated treatment for AS.
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Keywords {🔍}

autophagy, pubmed, article, google, scholar, cas, cell, cells, role, central, atherosclerotic, plaque, vascular, autophagic, death, effects, smcs, liu, inflammatory, formation, macrophages, plaques, activity, inflammation, endothelial, tabriz, data, membrane, response, inhibition, treatment, disease, activation, pathway, ecs, mtor, resveratrol, types, apoptosis, metformin, function, smooth, cardiovascular, lipid, stress, lysosomes, modulation, production, martinet, med,

Topics {✒️}

c-jun n-terminal kinase arrb1/β-arrestin-1 mediates neuroprotection macro/micro/chaperone-mediated vascular smooth-muscle cells inflammation-induced preterm labor drp1-mediated mitochondrial fission β-arrestin-1 significantly promotes tgf-β1-stimulated calcification double-edged sword activity article download pdf stress-related signals autophagy increased cell-substrate adhesion targeting pro-il-1β autophagic-induced cell death mir-30-mediated translational control newly-published document confirmed smooth muscle cells rac1-mtor signaling pathway western diet increased late-stage quality control de meyer gr proteomic profile autophagosomes prevents apoptosis reducing pro-inflammatory cytokines tnf-α regulate autophagy autophagy-related signaling pathway reduce pro-inflammatory status autophagy-deficient mouse models ampk/mtor signaling pathway autophagy-dependent cell death chaperone-mediated autophagy postpone severe vasculitis cell death induced protein-coupled receptors privacy choices/manage cookies reza rahbarghazi metformin suppresses diabetes-accelerated tnf-α production [19] plant-derived polyphenol arterial intima formed coronary arterial myocytes autophagy-induced elements promotes mitochondrial quality recent pharmacological study article hassanpour rabbit model results mitochondrial dna mediated reactive oxygen species creative commons license oxidized lipids found

Questions {❓}

Autophagy in cell death: an innocent convict?
Does autophagy contribute to cell death?
Role of autophagy in atherosclerosis: foe or friend?
Role of autophagy in atherosclerosis: foe or friend?

Schema {🗺️}

WebPage:
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         headline:Role of autophagy in atherosclerosis: foe or friend?
         description:Athrosclerosis is conceived as a chronic inflammatory status affecting cells from vascular walls. Different mechanisms and pathological features are evident at the onset of atherosclerotic changes via the engaging different cells from the vascular wall and circulatory cells. Attempts are currently focused on the detection of cell compensatory mechanisms against atherosclerotic changes to restore cell function and/or postpone severe vasculitis. Autophagy is an intracellular self-digesting process commonly protrudes exhausted organelles and injured cytoplasmic constituents via double-lipid bilayer membrane vesicles out the target cells. Recent investigations point to the critical and defensive role of autophagy in the vascular cells behavioral function such as endothelial cells and smooth muscle cells against different insults. Autophagy response and related effectors could be modulated in the favor to restore cell function and reduce pro-inflammatory status under pathological conditions. In this review, the recent findings were collected regarding the role of autophagy during atherosclerotic changes. We aimed to answer the question of how autophagy stimulation and/or inhibition could provide a promising effect on developing a sophisticated treatment for AS.
         datePublished:2019-05-02T00:00:00Z
         dateModified:2019-05-02T00:00:00Z
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            Pharmacological intervention
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            Cytokines and Growth Factors
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            Pharmacology/Toxicology
            Gastroenterology
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      headline:Role of autophagy in atherosclerosis: foe or friend?
      description:Athrosclerosis is conceived as a chronic inflammatory status affecting cells from vascular walls. Different mechanisms and pathological features are evident at the onset of atherosclerotic changes via the engaging different cells from the vascular wall and circulatory cells. Attempts are currently focused on the detection of cell compensatory mechanisms against atherosclerotic changes to restore cell function and/or postpone severe vasculitis. Autophagy is an intracellular self-digesting process commonly protrudes exhausted organelles and injured cytoplasmic constituents via double-lipid bilayer membrane vesicles out the target cells. Recent investigations point to the critical and defensive role of autophagy in the vascular cells behavioral function such as endothelial cells and smooth muscle cells against different insults. Autophagy response and related effectors could be modulated in the favor to restore cell function and reduce pro-inflammatory status under pathological conditions. In this review, the recent findings were collected regarding the role of autophagy during atherosclerotic changes. We aimed to answer the question of how autophagy stimulation and/or inhibition could provide a promising effect on developing a sophisticated treatment for AS.
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      dateModified:2019-05-02T00:00:00Z
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         AS
         Pharmacological intervention
         Immunology
         Allergology
         Cytokines and Growth Factors
         Rheumatology
         Pharmacology/Toxicology
         Gastroenterology
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         type:PostalAddress
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      address:
         name:Cardiovascular Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
         type:PostalAddress
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      address:
         name:Department of Cardiac Surgery, Shahid Madani Heart Hospital, Tabriz University of Medical Sciences, Tabriz, Iran
         type:PostalAddress
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            address:
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            name:Tabriz University of Medical Sciences
            address:
               name:Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
               type:PostalAddress
            type:Organization
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      url:http://orcid.org/0000-0003-3864-9166
      affiliation:
            name:Tabriz University of Medical Sciences
            address:
               name:Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
               type:PostalAddress
            type:Organization
            name:Tabriz University of Medical Sciences
            address:
               name:Department of Applied Cell Sciences, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran
               type:PostalAddress
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      name:Mohammad Nouri
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            name:Tabriz University of Medical Sciences
            address:
               name:Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Nasser Aghamohammadzadeh
      affiliation:
            name:Tabriz University of Medical Sciences
            address:
               name:Endocrine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
               type:PostalAddress
            type:Organization
      name:Nasser Safaei
      affiliation:
            name:Tabriz University of Medical Sciences
            address:
               name:Cardiovascular Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
               type:PostalAddress
            type:Organization
            name:Tabriz University of Medical Sciences
            address:
               name:Department of Cardiac Surgery, Shahid Madani Heart Hospital, Tabriz University of Medical Sciences, Tabriz, Iran
               type:PostalAddress
            type:Organization
      name:Mahdi Ahmadi
      affiliation:
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            address:
               name:Department of Physiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
               type:PostalAddress
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      name:Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
      name:Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
      name:Department of Applied Cell Sciences, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran
      name:Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
      name:Endocrine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
      name:Cardiovascular Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
      name:Department of Cardiac Surgery, Shahid Madani Heart Hospital, Tabriz University of Medical Sciences, Tabriz, Iran
      name:Department of Physiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran

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