This review describes precisely the consequence of TGFbeta1 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 TGFbeta1 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, TGFbeta1 is a multifunctional cytokine. There are three fundamental
directions of its activities: I. TGFbeta1 regulates cell proliferation, growth, differentiation and cells movement. II. TGFbeta1 has immunomodulatory
effects. III. TGFbeta1 has profibrogenic effects. TGFbeta1 action can be local and systemic. This review describes TGFbeta1 in pathology:
colitis ulcerosa, Crohn’s disease, coeliac disease, diabetic nephropathy, diabetic retinopathy and diabetic foot, pulmonary hypertension,
and Alzheimer’s disease. TGFbeta1 and its receptors are also of interest to endocrinologists. Lack of TGFbeta1-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 TGFbeta1 activity is an integral part of the fibrotic processes occurring
in the response to injury. An increased TGFbeta1 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 TGFbeta1 and leads to the development of liver cirrhosis. The results of experimental procedures
and treatment known as anti-TGFbeta1 strategy acting against the fibrosis in various tissues leads to hope regarding the use of anti-TGFbeta1
strategy in clinical practice.

(Endokrynol Pol 2013; 64 (5): 384–396)