Effects of Etanercept on TNF-α Inhibition in Rats with Adenine-Induced Chronic Kidney Disease

Mendieta-Condado, Edgar; Villaseñor-Tapia, Elda Cristina; Gálvez-Gastélum, Francisco Javier; Yáñez-Sánchez, Irinea; Pizano-Martínez, Óscar; Canales-Aguirre, Alejandro A.; Márquez-Aguirre, Ana Laura

doi:10.1155/2022/4970753

Cited by 3 publications

(4 citation statements)

References 27 publications

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“…Etanercept was unsuccessful in preventing renal fibrosis that occurred 4 weeks into adenosine administration. Thus, more investigations need to be conducted to determine the effectiveness of TNF-α inhibitors on CKD [ 104 ].…”

Section: Ckd Managementmentioning

confidence: 99%

The Role of Inflammation in CKD

Kadatane

Satariano

Massey

et al. 2023

Cells

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Chronic kidney disease (CKD) affects many adults worldwide. Persistent low-grade inflammation is a substantial factor in its development and progression and has correlated with increased mortality and cardiovascular problems. This low-grade inflammation is a product of dysregulation of the normal balance between pro- and anti-inflammatory markers. Various factors such as increased innate immune system activation, reactive oxygen species production, periodontal disease, dysregulation of anti-inflammatory systems and intestinal dysbiosis result in the dysregulation of this balance. Furthermore, this low-grade inflammation has down-effects such as hypertension, renal fibrosis and acceleration of renal function decline. Moreover, low-grade inflammation over time has been linked to malignancy in CKD. As CKD progresses, many patients require dialysis, which has a negative bidirectional relationship with persistent inflammation. Treatment options for inflammation in CKD are vast, including cytokine inhibitors, statins and diets. However, more research is needed to create a standardized management plan. In this review, we will examine the normal physiology of the kidney and its relationship with the immune system. We will then delve into the pathology behind persistent inflammation, the various causes of inflammation, the downstream effects of inflammation, dialysis and potential treatments for inflammation in CKD.

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Section: Ckd Managementmentioning

confidence: 99%

The Role of Inflammation in CKD

Kadatane

Satariano

Massey

et al. 2023

Cells

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“…Serum TNFα levels are elevated in animal models of CKD, including nephrectomized rodents, Col4a3 −/− mice, and mice receiving an adenine-rich diet [176][177][178][179], as well as in patients with CKD [180]. TNFα stimulates the UPS [181] and when administered to rats increases protein degradation in skeletal muscle [182].…”

Section: Mechanisms Of Ckd-associated Sarcopeniamentioning

confidence: 99%

“…TNFα binds to the TNF type 1 receptor (TNFR1) located on the cell membrane of myofibers, resulting in the activation of nuclear factor κB (NFκB) and increases in the levels of reactive oxygen species (ROS), which then stimulates a wide array of pro-inflammatory gene programs, including the secretion of IL6 and IL1β [184][185][186][187][188][189]. Serum TNFα levels are elevated in animal models of CKD, including nephrectomized rodents, Col4a3 −/− mice, and mice receiving an adenine-rich diet [176][177][178][179], as well as in patients with CKD [180]. TNFα stimulates the UPS [181] and when administered to rats increases protein degradation in skeletal muscle [182].…”

Section: Mechanisms Of Ckd-associated Sarcopeniamentioning

confidence: 99%

Skeletal Muscle Injury in Chronic Kidney Disease—From Histologic Changes to Molecular Mechanisms and to Novel Therapies

Heitman,

Alexander,

Faul

2024

IJMS

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Chronic kidney disease (CKD) is associated with significant reductions in lean body mass and in the mass of various tissues, including skeletal muscle, which causes fatigue and contributes to high mortality rates. In CKD, the cellular protein turnover is imbalanced, with protein degradation outweighing protein synthesis, leading to a loss of protein and cell mass, which impairs tissue function. As CKD itself, skeletal muscle wasting, or sarcopenia, can have various origins and causes, and both CKD and sarcopenia share common risk factors, such as diabetes, obesity, and age. While these pathologies together with reduced physical performance and malnutrition contribute to muscle loss, they cannot explain all features of CKD-associated sarcopenia. Metabolic acidosis, systemic inflammation, insulin resistance and the accumulation of uremic toxins have been identified as additional factors that occur in CKD and that can contribute to sarcopenia. Here, we discuss the elevation of systemic phosphate levels, also called hyperphosphatemia, and the imbalance in the endocrine regulators of phosphate metabolism as another CKD-associated pathology that can directly and indirectly harm skeletal muscle tissue. To identify causes, affected cell types, and the mechanisms of sarcopenia and thereby novel targets for therapeutic interventions, it is important to first characterize the precise pathologic changes on molecular, cellular, and histologic levels, and to do so in CKD patients as well as in animal models of CKD, which we describe here in detail. We also discuss the currently known pathomechanisms and therapeutic approaches of CKD-associated sarcopenia, as well as the effects of hyperphosphatemia and the novel drug targets it could provide to protect skeletal muscle in CKD.

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“…Etanercept, a biological medication available under the brand names Enbrel and others, is used to treat autoimmune illnesses by inhibiting the inflammatory cytokine TNF-α. 72 The U.S. has permitted it to treat conditions like psoriatic arthritis, juvenile idiopathic arthritis, rheumatoid arthritis, plaque psoriasis, and ankylosing spondylitis. Food and Drug Administration (FDA).…”

Section: A Connection Between Blood Testosterone Levels and Testicula...mentioning

confidence: 99%

An Overview of the Mechanisms of Cadmium-induced Toxicity in the Male Reproductive System

Antar,

Halouani,

Gad

et al. 2023

Pharm Sci

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Cadmium (Cd) is a toxic heavy metal that is known to accumulate in various organs and tissues in the body, including the testes. Exposure to Cd has been shown to cause significant testicular damage, including impaired spermatogenesis and decreased fertility in both humans and animals. This damage is thought to be due to Cd-induced oxidative stress and inflammation, which can lead to cellular damage and apoptosis. Cd has also been shown to disrupt the blood-testis barrier, leading to increased permeability and an altered testicular microenvironment. In addition, Cd exposure has been linked to changes in hormone levels, including decreased testosterone production and altered gonadotropin secretion. Reactive oxygen species (ROS) and an imbalance in the activity of antioxidant enzymes cause oxidative stress. The nuclear factor kappa-B (NF-κB) signaling system, which controls multiple genes involved in inflammatory responses including tumor necrosis factor (TNF-α), is activated by oxidative stress. These effects can contribute to decreased sperm count, motility, and viability. Efforts to reduce exposure to Cd may help to prevent or mitigate the harmful effects on testicular function. This can be achieved through occupational and environmental regulations, as well as public education and awareness programs. In this review, we highlight many of the principal mechanisms included in testicular damage. These pathways could be considered promising targets for the development of potential therapies for a variety of important human diseases.

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Effects of Etanercept on TNF-α Inhibition in Rats with Adenine-Induced Chronic Kidney Disease

Cited by 3 publications

References 27 publications

The Role of Inflammation in CKD

The Role of Inflammation in CKD

Skeletal Muscle Injury in Chronic Kidney Disease—From Histologic Changes to Molecular Mechanisms and to Novel Therapies

An Overview of the Mechanisms of Cadmium-induced Toxicity in the Male Reproductive System

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