Angiogenic cytokines in renovascular disease: do they have potential for therapeutic use?

Alejandro R Chade1, Nicholas Stewart

  • 1Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216-4505, USA. achade@umc.edu

Insights

Damage to the renal microvasculature is an early step in chronic kidney disease. Targeting this damage with angiogenic cytokines may protect kidney function and slow disease progression.

Area of Science:

  • Nephrology
  • Vascular Biology
  • Regenerative Medicine

Background:

  • Renal microvascular damage is implicated in the early stages of chronic kidney disease (CKD).
  • Chronic renovascular disease is characterized by microvascular dysfunction, damage, and impaired angiogenesis, contributing to progressive renal dysfunction.
  • Protecting the renal microcirculation may slow or halt CKD progression.

Purpose of the Study:

  • To review the therapeutic potential of angiogenic cytokines for protecting the kidney microvasculature in chronic renovascular disease.
  • To assess the feasibility of using angiogenic factors to preserve renal function.

Main Methods:

  • Review of experimental and clinical studies on renal microvasculature in CKD.
  • Focus on the role of angiogenic cytokines like vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF).

Main Results:

  • Stimulation of vascular proliferation and repair using VEGF or HGF shows potential.
  • Evidence suggests these interventions can slow renal damage progression and stabilize renal function.
  • Angiogenic cytokine therapy may protect renal parenchyma.

Conclusions:

  • Targeting renal microvascular damage with angiogenic cytokines is a promising therapeutic strategy for CKD.
  • These therapies could potentially preserve renal function as a standalone treatment or an adjunct to existing therapies.
  • Further research is warranted to fully establish the efficacy and safety of angiogenic cytokine therapy in renovascular disease.

Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

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,...
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme (ECE). Of...