Tubulointerstitial injury: Signaling pathways, inflammation, fibrogenesis

Stella P. Hartono, Joseph P. Grande

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Scopus citations


Renovascular hypertension (RVH) is an important cause of both renal and cardiovascular morbidity and mortality. Atherosclerosis is the most common etiology underlying the development of RVH. In the stenotic kidney, the development of interstitial fibrosis and tubular atrophy is associated with the influx of inflammatory cells. These morphologic alterations result from a complex interplay of several pathways involving the renin angiotensin system, oxidative stress, the TGF-β-Smad signaling pathway, and the mitogen-activated protein kinase (MAPK) pathway, leading to both local and systemic production of chemokines that promote ongoing inflammation and interstitial fibrosis. In this chapter, we will summarize recent human and experimental studies to determine how these signaling pathways interact and contribute to renal inflammation and fibrogenesis. Identification of these pathways will provide a mechanistic basis for the development of RVH and may provide the basis for novel therapeutic targets directed towards arresting the progression of renal disease in patients with renal artery stenosis.

Original languageEnglish (US)
Title of host publicationRenal Vascular Disease
PublisherSpringer-Verlag London Ltd
Number of pages14
ISBN (Electronic)9781447128106
ISBN (Print)1447128095, 9781447128090
StatePublished - Dec 1 2014


  • CCL2
  • Fibrosis
  • Inflammation
  • MAPK
  • Macrophage
  • Renal artery stenosis
  • TGF-Β

ASJC Scopus subject areas

  • General Medicine


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