CCL2 as a microvascular "tone breaker": inflammatory signaling and the failure of kidney autoregulation in salt-sensitive hypertension

Kidney Int. 2026 Jun;109(6):1085-1088. doi: 10.1016/j.kint.2026.03.004.

Abstract

Hypertension-associated kidney injury is strongly shaped by the ability of the kidney to buffer systemic pressure at the afferent arteriole. Feng et al. identify C-C motif chemokine ligand 2 as a direct regulator of kidney microvascular smooth muscle contractility in Dahl salt-sensitive rats. Loss of C-C motif chemokine ligand 2 preserves Notch3-Mylk (myosin light-chain kinase) signaling, maintains myogenic tone, protects autoregulation, and prevents kidney injury. These findings position the C-C motif chemokine ligand 2/C-C motif chemokine receptor 2 axis as a mechanistic bridge between inflammatory signaling and hypertensive nephropathy.

MeSH terms

  • Animals
  • Chemokine CCL2* / metabolism
  • Homeostasis
  • Humans
  • Hypertension* / complications
  • Hypertension* / metabolism
  • Hypertension* / physiopathology
  • Hypertension, Renal* / etiology
  • Hypertension, Renal* / metabolism
  • Hypertension, Renal* / physiopathology
  • Inflammation
  • Kidney* / blood supply
  • Kidney* / physiopathology
  • Nephritis
  • Rats
  • Rats, Inbred Dahl
  • Receptors, Notch / metabolism
  • Signal Transduction
  • Sodium Chloride, Dietary / adverse effects

Substances

  • Chemokine CCL2
  • Sodium Chloride, Dietary
  • Receptors, Notch

Supplementary concepts

  • Hypertensive Nephropathy