Molecular Linkage between Immune System Disorders and Atherosclerosis

Napiórkowska-Baran, Katarzyna; Schmidt, Oskar; Szymczak, Bartłomiej; Lubański, Jakub; Doligalska, Agata; Bartuzi, Zbigniew

doi:10.3390/cimb45110552

Cited by 4 publications

(2 citation statements)

References 175 publications

(256 reference statements)

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“…Heart damage due to ischemia-reperfusion injury requires high NAD + to control the infarct size and prevent cardiac injury. The causes of CVDs such as cardiomyopathy [ 78 ], atherosclerosis [ 79 ], and heart failure [ 80 ] are also associated with metabolic disorders. Boosting NAD + levels through metabolism may help to improve these unwanted critical heart conditions.…”

Section: The Combined Effect Of Nampt Naprt and Nrkmentioning

confidence: 99%

The role of nicotinamide adenine dinucleotide salvage enzymes in cardioprotection

Kibria,

Das,

Arefin

2024

kitp

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The increasing trend of cardiac diseases is becoming a major threat globally. Cardiac activities are based on integrated action potential through electronic flux changes within intra- and extracellular molecular activities. Nicotinamide adenine dinucleotide (NAD) is a major electron carrier present in almost all living cells and creates gated potential by electron exchange from one chemical to another in terms of oxidation (NAD + ) and reduction (NADH) reactions. NAD + plays an important role directly or indirectly in protecting against various cardiovascular diseases, including heart failure, occlusion, ischemia-reperfusion (IR) injury, arrhythmia, myocardial infarction (MI), rhythmic disorder, and a higher order of cardiovascular complexity. Nicotinamide phosphoribosyl transferase (NAMPT) is well known as a rate-limiting enzyme in this pathway except for de-novo NAD synthesis and directly involved in the cardioprotective activity. There are two more enzymes – nicotinate phosphoribosyl transferase (NAPRT) and nicotinamide riboside kinase (NRK) – which also work as rate-limiting factors in the NAD+ synthesis pathway. This study concentrated on the role of NAMPT, NAPRT, and NRK in cardioprotective activity and prospective cardiac health.

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Section: The Combined Effect Of Nampt Naprt and Nrkmentioning

confidence: 99%

The role of nicotinamide adenine dinucleotide salvage enzymes in cardioprotection

Kibria,

Das,

Arefin

2024

kitp

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“…Pro-inflammatory M1 macrophages are the main inflammatory cell population in lipid cores [5,6]; they engulf oxidized low-density lipoprotein (LDL) cholesterol and transform into foam cells, are responsible for the formation of a necrotic core, and promote disease progression and plaque rupture. Anti-inflammatory M2 macrophages, on the other hand, phagocytize lipid particles and apoptotic cells, and stimulate plaque regression [7][8][9]. The dynamic evolution and stability of atherosclerotic plaques rely on both the quantity of infiltrated macrophages and their polarization state [7].…”

Section: Introductionmentioning

confidence: 99%

Ghrelin Expression in Atherosclerotic Plaques and Perivascular Adipose Tissue: Implications for Vascular Inflammation in Peripheral Artery Disease

Peiu,

Iosep,

Danciu

et al. 2024

JCM

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Atherosclerosis, a leading cause of peripheral artery disease (PAD), is driven by lipid accumulation and chronic inflammation within arterial walls. Objectives: This study investigates the expression of ghrelin, an anti-inflammatory peptide hormone, in plaque morphology and inflammation in patients with PAD, highlighting its potential role in age-related vascular diseases and metabolic syndrome. Methods: The analysis specifically focused on the immunohistochemical expression of ghrelin in atherosclerotic plaques and perivascular adipose tissue (PVAT) from 28 PAD patients. Detailed immunohistochemical staining was performed to identify ghrelin within these tissues, comparing its presence in various plaque types and assessing its association with markers of inflammation and macrophage polarization. Results: Significant results showed a higher prevalence of calcification in fibro-lipid plaques (63.1%) compared to fibrous plaques, with a notable difference in inflammatory infiltration between the two plaque types (p = 0.027). Complicated plaques exhibited increased ghrelin expression, suggesting a modulatory effect on inflammatory processes, although this did not reach statistical significance. The correlation between ghrelin levels and macrophage presence, especially the pro-inflammatory M1 phenotype, indicates ghrelin’s involvement in the inflammatory dynamics of atherosclerosis. Conclusions: The findings propose that ghrelin may influence plaque stability and vascular inflammation, pointing to its therapeutic potential in managing atherosclerosis. The study underlines the necessity for further research to clarify ghrelin’s impact on vascular health, particularly in the context of metabolic syndrome and age-related vascular alterations.

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