From Low-Grade Inflammation in Osteoarthritis to Neuropsychiatric Sequelae: A Narrative Review

Naumovs, Vladimirs; Groma, Valērija; Mednieks, Jānis

doi:10.3390/ijms232416031

Cited by 5 publications

(5 citation statements)

References 288 publications

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“…These factors further exacerbate cartilage damage and contribute to the chronic low-grade inflammation observed in knee OA. In OA, the increased proinflammatory factors can amplify the inflammatory response [29]. Chronic low-grade inflammation may result in the upregulation of cartilage catabolic factors and articular cartilage degradation [30].…”

Section: Discussionmentioning

confidence: 99%

PSD95 as a New Potential Therapeutic Target of Osteoarthritis: A Study of the Identification of Hub Genes through Self-Contrast Model

Huang,

Lin,

Shen

et al. 2023

IJMS

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Osteoarthritis (OA) is a worldwide joint disease. However, the precise mechanism causing OA remains unclear. Our primary aim was to identify vital biomarkers associated with the mechano-inflammatory aspect of OA, providing potential diagnostic and therapeutic targets for OA. Thirty OA patients who underwent total knee arthroplasty were recruited, and cartilage samples were obtained from both the lateral tibial plateau (LTP) and medial tibial plateau (MTP). GO and KEGG enrichment analyses were performed, and the protein–protein interaction (PPI) assessment was conducted for hub genes. The effect of PSD95 inhibition on cartilage degeneration was also conducted and analyzed. A total of 1247 upregulated and 244 downregulated DEGs were identified. Significant differences were observed between MTP and LTP in mechanical stress-related genes and activated sensory neurons based on a self-contrast model of human knee OA. Cluster analysis identified DLG4 as the hub gene. Cyclic loading stress increased PSD95 (encoded by DLG4) expression in LTP cartilage, and PSD95 inhibitors could alleviate OA progression. This study suggests that inhibiting PSD95 could be a potential therapeutic strategy for preventing articular cartilage degradation.

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Section: Discussionmentioning

confidence: 99%

PSD95 as a New Potential Therapeutic Target of Osteoarthritis: A Study of the Identification of Hub Genes through Self-Contrast Model

Huang,

Lin,

Shen

et al. 2023

IJMS

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“…Chronic low-grade inflammatory disorders are often associated with conditions such as atherosclerosis, obesity, IR, osteoarthritis and neuropsychiatric diseases. 33 IR and relative insulin deficiency caused by pancreatic β-cell dysfunction form the principal pathology of T2D. 34 Inflammatory disorders in T2D are advanced due to the dysregulation of immune cells, and oxidative stress.…”

Section: Methods and Search Strategymentioning

confidence: 99%

“…Chronic low‐grade inflammatory disorders involve the presence of low levels of proinflammatory/inflammatory cytokines and their genes. Chronic low‐grade inflammatory disorders are often associated with conditions such as atherosclerosis, obesity, IR, osteoarthritis and neuropsychiatric diseases 33 . IR and relative insulin deficiency caused by pancreatic β‐cell dysfunction form the principal pathology of T2D 34 .…”

Section: Effects Of T2d On Depressionmentioning

confidence: 99%

Depression and type 2 diabetes: A causal relationship and mechanistic pathway

Khawagi,

Al‐kuraishy,

Hussein

et al. 2024

Diabetes Obesity Metabolism

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Depression is a mood disorder that may increase risk for the development of insulin resistance (IR) and type 2 diabetes (T2D), and vice versa. However, the mechanistic pathway linking depression and T2D is not fully elucidated. The aim of this narrative review, therefore, was to discuss the possible link between depression and T2D. The coexistence of T2D and depression is twice as great compared to the occurrence of either condition independently. Hyperglycaemia and dyslipidaemia promote the incidence of depression by enhancing inflammation and reducing brain serotonin (5‐hydroxytryptamine [5HT]). Dysregulation of insulin signalling in T2D impairs brain 5HT signalling, leading to the development of depression. Furthermore, depression is associated with the development of hyperglycaemia and poor glycaemic control. Psychological stress and depression promote the development of T2D. In conclusion, T2D could be a potential risk factor for the development of depression through the induction of inflammatory reactions and oxidative stress that affect brain neurotransmission. In addition, chronic stress in depression may induce the development of T2D through dysregulation of the hypothalamic–pituitary–adrenal axis and increase circulating cortisol levels, which triggers IR and T2D.

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“…This SNS-mediated increased pro-inflammatory tone may be capable to promote inflammation-induced cartilage catabolism in OA. On the other hand, the chronic low-grade inflammatory status in OA has been shown to alter behavior [ 219 ]. Depression and obesity are common comorbidities in patients with knee OA.…”

Section: Sympathetic Influence On Mild Chronic Inflammatory Diseasesmentioning

confidence: 99%

Role of the Sympathetic Nervous System in Mild Chronic Inflammatory Diseases: Focus on Osteoarthritis

Sohn¹,

Jenei-Lanzl²

2023

Neuroimmunomodulation

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The sympathetic nervous system (SNS) is a major regulatory mediator connecting the brain and the immune system that influences accordingly inflammatory processes within the entire body. In the periphery, the SNS exerts its effects mainly via its neurotransmitters norepinephrine (NE) and epinephrine (E), which are released by peripheral nerve endings in lymphatic organs and other tissues. Depending on their concentration, NE and E bind to specific α- and β-adrenergic receptor subtypes and can cause both pro- and anti-inflammatory cellular responses. The co-transmitter neuropeptide Y, adenosine triphosphate, or its metabolite adenosine are also mediators of the SNS. Local pro-inflammatory processes due to injury or pathogens lead to an activation of the SNS, which in turn induces several immunoregulatory mechanisms with either pro- or anti-inflammatory effects depending on neurotransmitter concentration or pathological context. In chronic inflammatory diseases, the activity of the SNS is persistently elevated and can trigger detrimental pathological processes. Recently, the sympathetic contribution to mild chronic inflammatory diseases like osteoarthritis (OA) has attracted growing interest. OA is a whole-joint disease and is characterized by mild chronic inflammation in the joint. In this narrative article, we summarize the underlying mechanisms behind the sympathetic influence on inflammation during OA pathogenesis. In addition, OA comorbidities also accompanied by mild chronic inflammation, such as hypertension, obesity, diabetes, and depression, will be reviewed. Finally, the potential of SNS-based therapeutic options for the treatment of OA will be discussed.

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From Low-Grade Inflammation in Osteoarthritis to Neuropsychiatric Sequelae: A Narrative Review

Cited by 5 publications

References 288 publications

PSD95 as a New Potential Therapeutic Target of Osteoarthritis: A Study of the Identification of Hub Genes through Self-Contrast Model

PSD95 as a New Potential Therapeutic Target of Osteoarthritis: A Study of the Identification of Hub Genes through Self-Contrast Model

Depression and type 2 diabetes: A causal relationship and mechanistic pathway

Role of the Sympathetic Nervous System in Mild Chronic Inflammatory Diseases: Focus on Osteoarthritis

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