Journals / Türk Nefroloji Diyaliz ve Transplantasyon Dergisi / 2013 / Cilt: 22 - Sayı: 3

Böbrek hastalarında ateroskleroz gelişiminde yeni bir oyuncu: tumor necrosis factor-like weak ınducer of apoptosis (tweak)

A Novel player in atherosclerotic diseases in renal patients: tumor necrosis factor-like weak ınducer of apoptosis (tweak)

Pages
235–237
Publication Date
2022-11-05
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

This review focuses on the association of TWEAK with atherosclerosis in patients with enal patients.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Cardiovascular disease is common in patients with chronic kidney disease.
📊
Key Findings & Data:While it is known that TWEAK levels are decreased in patient with renal failure, its association with atherosclerosis is not well-defined.
💡
Conclusion & Impact:This review focuses on the association of TWEAK with atherosclerosis in patients with enal patients.
🔬Design:Review & Systematic Survey
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Cardiovascular disease is common in patients with chronic kidney disease. Atherosclerosis has a very mportant role in pathogenesis of cardiovascular diseases. Tumor Necrosis factor- Like Weak Inducer of Apoptosis (TWEAK) is a glycoprotein that belongs to the TNF superfamily. TWEAK plays important oles in cellular proliferation, growth, migration, osteoclastogenesis, angiogenesis and apoptosis. In he recent years, TWEAK has been suggested to have a role in atherosclerosis. While it is known that TWEAK levels are decreased in patient with renal failure, its association with atherosclerosis is not well-defined. This review focuses on the association of TWEAK with atherosclerosis in patients with enal patients.

Özet

Kronik böbrek yetmezliği hastalarında kardiyovasküler olaylar sık görülür. Ateroskleroz, kardiyovasküler olayların patogenezinde önemli bir yere sahiptir. Tumor Necrosis factor- Like Weak Inducer of Apoptosis (TWEAK) TNF süper familyasına ait bir glikoproteindir. TWEAK organizmada hücresel büyüme, proliferasyon, migrasyon, osteoklastogenezis, anjiogenezis ve apoptoziste rol oynar. Son zamanlarda TWEAKin ateroskleroz gelişiminde de rol oynayabileceği ileri sürülmüştür. Böbrek yetmezliği durumlarında TWEAK düzeylerinin azaldığı bilinirken renal hasta popülasyonunda TWEAK-ateroskleroz ilişkisi netlik kazanmamıştır. Bu derlemede böbrek hastalarında TWEAK- ateroskleroz ilişkisi gözden geçirilmiştir.

🔖

Cite This Article

GÜNGÖR, Ö., YILMAZ, M. İ., TÖZ, H. (2022). Böbrek hastalarında ateroskleroz gelişiminde yeni bir oyuncu: tumor necrosis factor-like weak ınducer of apoptosis (tweak). Türk Nefroloji Diyaliz ve Transplantasyon Dergisi, Cilt: 22 - Sayı: 3, 235–237. https://ajindex.com/articles/636361

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (13)

  1. Kopyt N: Management and treatment of chronic kidney disease. Nurse Pract 2007; 32: 14-23
  2. Sidhu MS, Dellsperger KC: Cardiovascular problems in dialysis patients: Impact on survival. Adv Perit Dial 2010; 26: 47-52
  3. Weber C, Noels H: Atherosclerosis: Current pathogenesis and therapeutic options. Nat Med 2011; 17: 1410-1422
  4. Yılmaz MI, Çağlar K, Sağlam M, Eyileten T, Sonmez A, Açıkel C, Özgürtaş T, Oğuz Y, Vural A, Yenicesu M: Endothelial dysfunction in chronic renal disease; The role of adiponectin and inflammation. Turk Neph Dial Transpl 2007; 16(2): 54-62
  5. Braunersreuther V, Mach F, Steffens S: The specific role of chemokines in atherosclerosis. Thromb Haemost 2007; 97: 714-21
  6. Wiley SR, Winkles JA: TWEAK, a member of the TNF superfamily, is a multifunctional cytokine that binds the TWEAKR/Fn14 receptor. Cytokine Growth Factor Rev 2003; 14: 241–249 Burkly LC, Michaelson JS, Hahm K, Jakubowski A, Zheng TS: TWEAKing tissue remodeling by a multifunctional cytokine: Role of TWEAK/Fn14 pathway in health and disease. Cytokine 2007; 40: 1-16
  7. Moreno JA, Muñoz-García B, Martín-Ventura JL, Madrigal-Matute J, Orbe J, Páramo JA, Ortega L, Egido J, Blanco-Colio LM: The CD163-expressing macrophages recognize and internalize TWEAK: Potential consequences in atherosclerosis. Atherosclerosis 2009; 207: 103-110
  8. Saas P, Boucraut J, Walker PR, Quiquerez AL, BillotDesplat-Jego S, Chicheportiche Y, Dietrich PY: TWEAK stimulation of astrocytes and the proinflammatory consequences. Glia 2000; 32(1): 102-107
  9. Justo P, Sanz AB, Sanchez-Nino MD, Winkles JA, Lorz C, EgidoOrtiz A: Cytokine cooperation in renal tubular cell injury: Theof TWEAK. Kidney Int 2006; 70: 1750-1758
  10. Gao HX, Campbell SR, Burkly LC, Jakubowski A, JarchumBanas B, Saleem MA, Mathieson PW, Berman JW, Michaelson JS, Putterman C: TNF-like weak inducer of apoptosis (TWEAK) induces inflammatory and proliferative effects in human kidney cells. Cytokine 2009; 46: 24-35
  11. Chicheportiche Y, Chicheportiche R, Sizing I, ThompsonBenjamin CB, Ambrose C, Dayer JM: Proinflammatory activityTWEAK on human dermal fibroblasts and synoviocytes: Blocking and enhancing effects of anti-TWEAK monoclonal antibodies. Arthritis Res 2002; 4: 126-133
  12. Kralisch S, Ziegelmeier M, Bachmann A, Seeger J Lössner U, Blüher M, Stumvoll M, Fasshauer M: Serum levels of the atherosclerosis biomarkers TWEAK are decreased in type 2 diabetes and end-stage renal disease. Atherosclerosis 2008; 199: 440-444
  13. Blanco-Colio LM, Martín-Ventura JL, Muñóz-García B, OrbePára