Figures & data
Figure 1 The linear pathway leading from insulin deficiency, through hyperglycemia to diabetes complications.
![Figure 1 The linear pathway leading from insulin deficiency, through hyperglycemia to diabetes complications.](/cms/asset/47e944af-8e06-4ded-8ae5-4ed11d81cae5/dvhr_a_1991_f0001_b.jpg)
Figure 2 Schematic diagram indicating how hemodynamic and metabolic factors, and growth factors, can network to cause tissue damage. Inflammation and fibrosis occur variably in tissue at different stages of diabetes complications.
![Figure 2 Schematic diagram indicating how hemodynamic and metabolic factors, and growth factors, can network to cause tissue damage. Inflammation and fibrosis occur variably in tissue at different stages of diabetes complications.](/cms/asset/9380db2d-3b89-443b-8418-f9c622ac7ca0/dvhr_a_1991_f0002_b.jpg)
Figure 3 The major growth factors implicated in diabetes complications. The prosclerotic ones involved in human diabetic fibrosis are currently thought to be TGF-β and CTGF.
![Figure 3 The major growth factors implicated in diabetes complications. The prosclerotic ones involved in human diabetic fibrosis are currently thought to be TGF-β and CTGF.](/cms/asset/9f141656-cda5-409c-99ec-221843338099/dvhr_a_1991_f0003_b.jpg)
Figure 4 One pathogenic pathway by which high glucose in diabetes and hypertension work through prosclerotic growth factors to dysregulate ECM turnover. Both TGF-β and CTGF have been shown to induce TIMP-1 and PAI-1, resulting in reduced MMP and plasmin activity. This paradigm best applies to diabetic renal disease.
![Figure 4 One pathogenic pathway by which high glucose in diabetes and hypertension work through prosclerotic growth factors to dysregulate ECM turnover. Both TGF-β and CTGF have been shown to induce TIMP-1 and PAI-1, resulting in reduced MMP and plasmin activity. This paradigm best applies to diabetic renal disease.](/cms/asset/d836fe09-cb8e-4f71-a5e8-a0da77d98861/dvhr_a_1991_f0004_b.jpg)