Transforming growth factor β1 (TGFβ1) in physiology and pathology.

This review describes precisely the consequence of TGFβ1 prevalence in the organism, and its significant influence on physiological and pathophysiological processes. Organ and tissue distinctiveness hinder unambiguous characterisation of the cytokine. However, there are constant functions of TGFβ1 inducing no controversy: it participates in foetal development, control of cell growth and differentiation, induces fibrosis and scar formation (the process of 'wound healing'), causes the suppression of immune response, is involved in angiogenesis, the development of tumours, and inflammatory processes. Thus, TGFβ1 is a multifunctional cytokine. There are three fundamental directions of its activities: I. TGFβ1 regulates cell proliferation, growth, differentiation and cells movement. II. TGFβ1 has immunomodulatory effects. III. TGFβ1 has profibrogenic effects. TGFβ1 action can be local and systemic. This review describes TGFβ1 in pathology: colitis ulcerosa, Crohn's disease, coeliac disease, diabetic nephropathy, diabetic retinopathy and diabetic foot, pulmonary hypertension, and Alzheimer's disease. TGFβ1 and its receptors are also of interest to endocrinologists. Lack of TGFβ1-dependent growth control may result in oncogenesis: papillary, follicular and anaplastic thyroid cancers, prostate, breast and uterine cervical cancer, oesophagus, gastric, colorectal and liver cancers, NSCLC, and malignant melanoma. Excessive TGFβ1 activity is an integral part of the fibrotic processes occurring in the response to injury. An increased TGFβ1 expression has been observed in patients with pulmonary, kidney, and liver fibrosis. In chronic hepatitis, the prolonged stimulation of hepatic stellate cells being the result of chronic damage to hepatocytes results in the release of profibrogenic abundant factors such as TGFβ1 and leads to the development of liver cirrhosis. The results of experimental procedures and treatment known as anti-TGFβ1 strategy acting against the fibrosis in various tissues leads to hope regarding the use of anti-TGFβ1 strategy in clinical practice.