PMC:7335494 / 3344-4873 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7335494","sourcedb":"PMC","sourceid":"7335494","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7335494","text":"Under physiological conditions, inflammation is a response to harmful stimuli (pathogens or tissue lesions), a cellular adaptive mechanism aiming to restore tissue homeostasis (Medzhitov, 2008). Inflammatory responses are self-limited through specific checkpoints that curb the progression and promote the resolution of inflammation (Basil and Levy, 2016; Serhan and Savill, 2005). Failure due to the deleterious alterations of the inflammatory pathways brings about the excessive release of pro-inflammatory molecules, leading to chronic low-grade inflammation and fibrosis (Norling and Serhan, 2010; Russell and Schwarze, 2014). The persistence of this usually short-term defence mechanism leads to a chronic inflammatory state, transitioning from solution to cause, becoming in fact a lesion-inducing factor for the affected tissues. This may be a result of the dysregulation of several cellular pathways involving cyclooxygenase-2 (COX-2), signal transducer and activator of transcription 3 (STAT3), matrix metalloproteinase-9 (MMP-9), nuclear factor kappa-B (NF-κB), cytokines with inflammatory outcome: interleukins (IL-1, IL-6, IL-8), tumour necrosis factor alpha (TNF-α), cell adhesion molecules and chemokines, etc. Of note, the resolution of the inflammatory process cannot be simply switched off by restricting the synthesis of the pro-inflammatory molecules, requiring cellular intervention through anti-inflammatory and pro-resolving molecules (Minihane et al., 2015; Ortega-Gomez et al., 2013; Serhan et al., 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