It is commonly believed that the inactivation of inflammation is mainly due to the decay or cessation of inducers. In reality, in connection with the development of atherosclerosis, spontaneous decay of inducers is not observed. It is now known that lipid mediators originating from polyunsaturated fatty acids (PUFAs), which are important constituents of all cell membranes, can act in the inflamed tissue and bring it to resolution. In fact, PUFAs, such as arachidonic acid (AA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), are precursors to both pro-inflammatory and anti-inflammatory compounds. In this review, we describe the lipid mediators of vascular inflammation and resolution, and their biochemical activity. In addition, we highlight data from the literature that often show a worsening of atherosclerotic disease in subjects deficient in lipid mediators of inflammation resolution, and we also report on the anti-proteasic and anti-thrombotic properties of these same lipid mediators. It should be noted that despite promising data observed in both animal and in vitro studies, contradictory clinical results have been observed for omega-3 PUFAs. Many further studies will be required in order to clarify the observed conflicts, although lifestyle habits such as smoking or other biochemical factors may often influence the normal synthesis of lipid mediators of inflammation resolution.

Thyroid Hormones (THs) play a central role in the development, cell growth, differentiation, and metabolic homeostasis of neurosensory systems, including the retina. The coordinated activity of various components of TH signaling, such as TH receptors (THRs) and the TH processing enzymes deiodinases 2 and 3 (DIO2, DIO3), is required for proper retinal maturation and function of the adult photoreceptors, Müller glial cells, and pigmented epithelial cells. Alterations of TH homeostasis, as observed both in frank or subclinical thyroid disorders, have been associated with sight-threatening diseases leading to irreversible vision loss i.e., diabetic retinopathy (DR), and age-related macular degeneration (AMD). Although observational studies do not allow causal inference, emerging data from preclinical models suggest a possible correlation between TH signaling imbalance and the development of retina disease. In this review, we analyze the most important features of TH signaling relevant to retinal development and function and its possible implication in DR and AMD etiology. A better understanding of TH pathways in these pathological settings might help identify novel targets and therapeutic strategies for the prevention and management of retinal disease.

Background/Objectives: Atherosclerosis and diabetes are largely recognized as inflammatory disorders and several inflammatory markers are used in clinical settings. Here we investigate the link of interleukin-6 (IL-6), C-Reactive Protein (CRP) and fibrinogen (FIB) with predisposing factors for atherosclerosis and diabetes; NT-pro-BNP, glycemia, insulin resistance, HDL and LDL respectively. Methods: the literature was collected using PubMed database. Results: CRP provides complementary information to NT-pro-BNP for high risk for major adverse cardiac events (MACE) in post-MI patients. CRP predicts cardiovascular and mortality in type 2 diabetic subjects. CRP binds to LDL triggering structural changes in HDL. CRP is also found in atheromatous plaque. IL-6 is a predictor of incident heart failure (HF) and IL-6 inhibition reduces HF hospitalization. IL-6 is related to a greater body mass index, NT–pro-BNP levels and insulin resistance. By blocking IL-6 may be a strategy for insulin resistance treatment. IL-6 levels correlate with endothelial dysfunction and carotid intima-media thickness, activating LDL-Receptor transcription. The FIB-to-albumin ratio in HF is positively correlated with NT-pro-BNP. Diabetic patients and insulin resistance condition could be related to hyperfibrinogenemia. The glycation level in the fibrinogen molecule is 2–3-fold higher in type 2 diabetic than in non-diabetic individuals, forming fibrin clots with enhanced resistance to fibrinolysis. Finally, because FIB is independently associated with the expression of a more atherogenic lipoprotein subfraction profile, it should be included in the assessment of coronary risk factors. Conclusions: CRP, IL-6 and FIB could be active players and potential targets for antiatherosclerotic and anti-diabetic therapies.