We are analyzing https://link.springer.com/article/10.1007/s12035-024-04060-4.

Title:
Mechanism of Efferocytosis in Determining Ischaemic Stroke Resolution—Diving into Microglia/Macrophage Functions and Therapeutic Modality | Molecular Neurobiology
Description:
After ischaemic cerebral vascular injury, efferocytosis—a process known as the efficient clearance of apoptotic cells (ACs) by various phagocytes in both physiological and pathological states—is crucial for maintaining central nervous system (CNS) homeostasis and regaining prognosis. The mechanisms of efferocytosis in ischaemic stroke and its influence on preventing inflammation progression from secondary injury were still not fully understood, despite the fact that the fundamental process of efferocytosis has been described in a series of phases, including AC recognition, phagocyte engulfment, and subsequent degradation. The genetic reprogramming of macrophages and brain-resident microglia after an ischaemic stroke has been equated by some researchers to that of the peripheral blood and brain. Based on previous studies, some molecules, such as signal transducer and activator of transcription 6 (STAT6), peroxisome proliferator-activated receptor γ (PPARG), CD300A, and sigma non-opioid intracellular receptor 1 (SIGMAR1), were discovered to be largely associated with aspects of apoptotic cell elimination and accompanying neuroinflammation, such as inflammatory cytokine release, phenotype transformation, and suppressing of antigen presentation. Exacerbated stroke outcomes are brought on by defective efferocytosis and improper modulation of pertinent signalling pathways in blood-borne macrophages and brain microglia, which also results in subsequent tissue inflammatory damage. This review focuses on recent researches which contain a number of recently discovered mechanisms, such as studies on the relationship between benign efferocytosis and the regulation of inflammation in ischaemic stroke, the roles of some risk factors in disease progression, and current immune approaches that aim to promote efferocytosis to treat some autoimmune diseases. Understanding these pathways provides insight into novel pathophysiological processes and fresh characteristics, which can be used to build cerebral ischaemia targeting techniques.
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Keywords {🔍}

pubmed, article, google, scholar, cas, central, cell, efferocytosis, stroke, cells, apoptotic, liu, immunol, zhang, wang, macrophage, ischemic, macrophages, injury, biol, phagocytosis, inflammation, chen, nat, clearance, brain, microglia, mol, receptor, polarization, role, pathway, neuroinflammation, zhao, sci, rev, res, zhu, cerebral, promotes, signaling, death, blood, nature, activation, therapeutic, inflammatory, immune, resolution, atherosclerosis,

Topics {✒️}

p38/mapk/ar-dependent pathway month download article/chapter gpr41/gβγ/pi3k/akt pathway gm-csf-differentiated human macrophages mesenchymal stem cells intranuclear nuclear factor-kappab hormone-induced cell death cerebral ischaemia-reperfusion injury central nervous system age-related immune alterations basophilic leukemia rbl-2h3 enhancing vegf-pi3k/akt sigma-1 receptor-regulated efferocytosis synaptotagmin vii-dependent delivery pi3k/akt/mtor pathway elmo/dock180/rac module junb/jnk/nf-κb phosphatidylserine-dependent homeostatic response slc7a11/gpx4 signaling pathway pten/pi3k/akt pathway sox5/pi3k/akt pathways lung-brain axis involved jak/stat/socs signalling anti-inflammatory oxysterol production sigma-1 receptor-modulated neuroinflammation accepted manuscript version full article pdf activating pi3k/akt/nrf2 vegf-mek1/2/erk1/2 signaling cholesterol-induced death attenuates brain atrophy de juan-sanz restores blood flow rna sequencing reveals shan-shan dong unique microglia type ru-juan liu pi3k/akt pathway m1/m2 polarization pi3k/akt/mtor privacy choices/manage cookies age-related deficits human cd300a binds chekeni fb microglia/macrophage functions infiltrating myeloid cells peripheral immune system article xie nf-κb pathway related subjects

Questions {❓}

Hodge S, Matthews G, Dean MM, Ahern J, Djukic M, Hodge G et al (2010) Therapeutic role for mannose-binding lectin in cigarette smoke-induced lung inflammation?
Rollini F, Franchi F, Angiolillo DJ (2017) Drug-drug interactions when switching between intravenous and oral P2Y(12) receptor inhibitors: how real is it?
Walter K (2022) What is acute ischemic stroke?

Schema {🗺️}

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         headline:Mechanism of Efferocytosis in Determining Ischaemic Stroke Resolution—Diving into Microglia/Macrophage Functions and Therapeutic Modality
         description:After ischaemic cerebral vascular injury, efferocytosis—a process known as the efficient clearance of apoptotic cells (ACs) by various phagocytes in both physiological and pathological states—is crucial for maintaining central nervous system (CNS) homeostasis and regaining prognosis. The mechanisms of efferocytosis in ischaemic stroke and its influence on preventing inflammation progression from secondary injury were still not fully understood, despite the fact that the fundamental process of efferocytosis has been described in a series of phases, including AC recognition, phagocyte engulfment, and subsequent degradation. The genetic reprogramming of macrophages and brain-resident microglia after an ischaemic stroke has been equated by some researchers to that of the peripheral blood and brain. Based on previous studies, some molecules, such as signal transducer and activator of transcription 6 (STAT6), peroxisome proliferator-activated receptor γ (PPARG), CD300A, and sigma non-opioid intracellular receptor 1 (SIGMAR1), were discovered to be largely associated with aspects of apoptotic cell elimination and accompanying neuroinflammation, such as inflammatory cytokine release, phenotype transformation, and suppressing of antigen presentation. Exacerbated stroke outcomes are brought on by defective efferocytosis and improper modulation of pertinent signalling pathways in blood-borne macrophages and brain microglia, which also results in subsequent tissue inflammatory damage. This review focuses on recent researches which contain a number of recently discovered mechanisms, such as studies on the relationship between benign efferocytosis and the regulation of inflammation in ischaemic stroke, the roles of some risk factors in disease progression, and current immune approaches that aim to promote efferocytosis to treat some autoimmune diseases. Understanding these pathways provides insight into novel pathophysiological processes and fresh characteristics, which can be used to build cerebral ischaemia targeting techniques.
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      description:After ischaemic cerebral vascular injury, efferocytosis—a process known as the efficient clearance of apoptotic cells (ACs) by various phagocytes in both physiological and pathological states—is crucial for maintaining central nervous system (CNS) homeostasis and regaining prognosis. The mechanisms of efferocytosis in ischaemic stroke and its influence on preventing inflammation progression from secondary injury were still not fully understood, despite the fact that the fundamental process of efferocytosis has been described in a series of phases, including AC recognition, phagocyte engulfment, and subsequent degradation. The genetic reprogramming of macrophages and brain-resident microglia after an ischaemic stroke has been equated by some researchers to that of the peripheral blood and brain. Based on previous studies, some molecules, such as signal transducer and activator of transcription 6 (STAT6), peroxisome proliferator-activated receptor γ (PPARG), CD300A, and sigma non-opioid intracellular receptor 1 (SIGMAR1), were discovered to be largely associated with aspects of apoptotic cell elimination and accompanying neuroinflammation, such as inflammatory cytokine release, phenotype transformation, and suppressing of antigen presentation. Exacerbated stroke outcomes are brought on by defective efferocytosis and improper modulation of pertinent signalling pathways in blood-borne macrophages and brain microglia, which also results in subsequent tissue inflammatory damage. This review focuses on recent researches which contain a number of recently discovered mechanisms, such as studies on the relationship between benign efferocytosis and the regulation of inflammation in ischaemic stroke, the roles of some risk factors in disease progression, and current immune approaches that aim to promote efferocytosis to treat some autoimmune diseases. Understanding these pathways provides insight into novel pathophysiological processes and fresh characteristics, which can be used to build cerebral ischaemia targeting techniques.
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