Pathophysiology and Angiogenesis in Chronic Kidney Disease
Summary
The pathophysiology of chronic kidney disease hinges on an interplay between fibrotic processes, microvascular injury and maladaptive repair. Progressive nephron loss leads to glomerulosclerosis and tubulointerstitial fibrosis, driven by persistent inflammation, oxidative stress and extracellular matrix accumulation. Microvascular rarefaction worsens hypoxia in both cortex and medulla, compromising oxygen and nutrient delivery. Angiogenesis in chronic kidney disease is marked by an imbalance between pro- and anti-angiogenic signals: reductions in vascular endothelial growth factor pathways and endothelial survival cues are accompanied by elevated anti-angiogenic mediators, tipping the equilibrium towards capillary loss. Dysregulated crosstalk among endothelial cells, pericytes and tubular epithelium further undermines vascular regeneration. Therapeutic strategies that restore angiogenic signalling or safeguard the endothelial niche aim to preserve microvascular integrity, attenuate fibrosis and slow functional decline.
Research from Nature Portfolio
Recent studies have employed multi-omic profiling in models of compensatory hypertrophy to identify lipid-sensing transcription factors as key modulators of renal growth. In particular, activation of peroxisome proliferator-activated receptor α within proximal tubule cells has been shown to orchestrate metabolic remodelling that supports nephron enlargement. These findings deepen our understanding of adaptive renal plasticity and suggest novel targets for modulating repair processes in chronic injury.
Pathophysiology and Angiogenesis in Chronic Kidney Disease publication trend
The graph below shows the total number of articles in pathophysiology and angiogenesis in chronic kidney disease across all publications each year (not limited to Nature Index journals).
Technical terms
Peritubular capillary rarefaction: The reduction in number and density of capillaries surrounding renal tubules, leading to tissue hypoxia.
Endothelial glycocalyx: A carbohydrate-rich layer on the luminal surface of endothelial cells that maintains vascular permeability and shear sensing.
Pericyte: A mural cell that stabilises microvessels and regulates endothelial proliferation and vessel maturation.
Peroxisome proliferator-activated receptor α (PPARα): A nuclear receptor that modulates lipid metabolism and cellular growth in proximal tubule cells.
Extracellular vesicle: A membrane-bound particle released by cells that transfers proteins, lipids and nucleic acids to target cells to modulate function.
References
- Signaling mechanisms in renal compensatory hypertrophy revealed by multi-omics. Nature Communications (2023).
- Endothelial Glycocalyx of Peritubular Capillaries in Experimental Diabetic Nephropathy: A Target of ACE Inhibitor-Induced Kidney Microvascular Protection. International Journal of Molecular Sciences (2023).
- Peritubular Capillary Rarefaction: An Underappreciated Regulator of CKD Progression. International Journal of Molecular Sciences (2020).
- Extracellular Vesicles Derived from Endothelial Progenitor Cells Protect Human Glomerular Endothelial Cells and Podocytes from Complement- and Cytokine-Mediated Injury. Cells (2021).
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