Fibrosis and SMAD signalling

Fibrosis and SMAD signalling

During normal physiological wound healing, inflammation, angiogenesis and fibrogenesis are all effectively controlled, so that once sufficient matrix has accumulated in the wound bed, matrix production ends and scarring is prevented. Should this response fail to resolve, or the tissue continues to receive injury, chronic fibrosis and scar tissue formation can occur.

The Biomarker Association between Depression and Vascular Disease

The Biomarker Association between Depression and Vascular Disease

Major depressive disorder (MDD) has repeatedly emerged as a confounding or prognostic factor in the development of cardiovascular pathologies and other common lifestyle diseases such as diabetes and obesity

Th17 Cells and IL-17: a possible link between inflammation and neuronal decline in Multiple Sclerosis

Th17 Cells and IL-17: a possible link between inflammation and neuronal decline in Multiple Sclerosis

Multiple sclerosis (MS) is an autoimmune and neurodegenerative disease of the central nervous system (CNS). A major component of the immunopathology of MS is the T cell-driven inflammatory attack from the peripheral immune system towards the CNS.

Macrophages transfer mitochondria to sensory neurons to resolve inflammatory pain

Macrophages transfer mitochondria to sensory neurons to resolve inflammatory pain

Inflammatory pain and hyperalgesia are considered functional features of an immune response, intended to protect tissue from further damage. At the affected site, immune cells and inflammatory mediators activate sensory neurons, resulting in pain signalling. The general consensus asserts that this pain passively resolves following cessation of the inflammatory stimulus. However, in many patients with chronic inflammatory diseases (such as rheumatoid arthritis and inflammatory bowel disease), resolution of inflammation does not translate to cessation of pain. This subsequently leads to chronic pain, where pain signals remain active for weeks to years, severely impacting a patient’s quality of life. The mechanism by which inflammatory pain is successfully resolved remains poorly understood.

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