Leptin: an entry point for the treatment of peripheral tissue fibrosis and related diseases
•Leptin is not only participates in the occurrence of liver fibrosis, but also has important significance in relieving liver fibrosis.•Leptin promotes lung, heart, and kidney fibrosis;•Leptin regulates adipose tissue fibrosis. Leptin is a small peptide mainly secreted by adipocyte, which acts on the...
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Veröffentlicht in: | International immunopharmacology 2022-05, Vol.106, p.108608-108608, Article 108608 |
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Sprache: | eng |
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Zusammenfassung: | •Leptin is not only participates in the occurrence of liver fibrosis, but also has important significance in relieving liver fibrosis.•Leptin promotes lung, heart, and kidney fibrosis;•Leptin regulates adipose tissue fibrosis.
Leptin is a small peptide mainly secreted by adipocyte, which acts on the central nervous system of the hypothalamus to regulate the body's energy balance by inhibiting food intake, it also can directly act on specific cells through leptin receptors (for example, ObRa, which exists in the blood–brain barrier or kidneys), thereby affect cell metabolism. Excessive deposition of extracellular matrix (ECM) causes damage to normal tissues or destruction of organ structure, which will eventually lead to tissue or organ fibrosis. The sustainable development of fibrosis can lead to structural damage and functional decline of organs, and even exhaustion, which seriously threatens human health and life. In recent years, studies have found that leptin directly alleviates the fibrosis process of various tissues and organs in mammals. Therefore, we speculate that leptin may become a significant treatment for fibrosis of various tissues and organs in the future. So, the main purpose of this review is to explore the specific mechanism of leptin in the process of fibrosis in multiple tissues and organs, and to provide a theoretical basis for the treatment of various tissues and organs fibrosis and related diseases caused by it, which is of great significance in the future. |
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ISSN: | 1567-5769 1878-1705 |
DOI: | 10.1016/j.intimp.2022.108608 |