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Related Concept Videos

Antihypertensive Drugs: Direct Renin Inhibitors01:25

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The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
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The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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5/6 Nephrectomy Using Sharp Bipolectomy Via Midline Laparotomy in Rats
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Targeting inerleukin-6 for renoprotection.

Ekaterina O Gubernatorova1,2, Mikhail Y Samsonov3, Marina S Drutskaya1,2,4

  • 1Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.

Frontiers in Immunology
|December 26, 2024
PubMed
Summary

Sterile inflammation drives kidney disease. Inhibiting Interleukin-6 (IL-6) signaling shows promise for treating acute and chronic kidney conditions, including transplantation, by reducing inflammation and protecting kidney function.

Keywords:
IL-6acute kidney injuryanti-cytokine therapychronic kidney diseaseinflammationkidney transplantationtrans-signaling

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Area of Science:

  • Nephrology
  • Immunology
  • Inflammation Research

Background:

  • Sterile inflammation is a key feature of non-infectious kidney diseases.
  • While inflammation aids tissue repair, excessive or prolonged responses cause kidney damage, nephron loss, and fibrosis.
  • Interleukin-6 (IL-6) is a critical cytokine in inflammation, signaling through classic and trans-signaling pathways.

Purpose of the Study:

  • To analyze the renoprotective potential of Interleukin-6 (IL-6) signaling inhibitors.
  • To evaluate therapeutic options in acute kidney injury, chronic kidney disease, and kidney transplantation.
  • To review current achievements and future prospects of IL-6 pathway suppression in kidney diseases.

Main Methods:

  • Review of existing therapeutic strategies targeting IL-6 signaling, including antibodies and small molecule inhibitors.
  • Analysis of animal data and clinical experience with IL-6 pathway inhibitors.
  • Focus on clinically relevant inhibitors and their application in various kidney disease models.

Main Results:

  • IL-6 signaling, via classic and trans-signaling, influences diverse cellular reactions in kidney injury.
  • Therapeutic agents like IL-6 neutralizing antibodies, JAK inhibitors, and soluble glycoprotein 130 variants are available.
  • Preclinical and clinical data suggest IL-6 suppression is a viable therapeutic strategy for kidney protection.

Conclusions:

  • Suppression of IL-6 signaling pathways holds significant therapeutic potential for acute and chronic kidney diseases.
  • Targeting IL-6 offers a promising approach to mitigate immune-mediated tissue damage and improve outcomes in kidney transplantation.
  • Further research into IL-6 inhibitors could lead to novel treatments for a range of renal conditions.