Fibrosis is a well-known pathological process in which several extracellular matrices (ECM), such as collagen, fibronectin, and elastin, abnormally accumulate in chronic inflamed and damaged tissues. Tissue fibrosis is the main cause of disability and death in many diseases. It affects various organs such as cardiovascular, lung, liver, and kidney. Currently, there are a few treatment strategies available for the prevention of fibrosis.

Although the mechanisms of various fibrotic diseases are different, the common feature of tissues affected by fibrosis is the presence of excessive activated fibroblasts and transformed myofibroblasts. In the occurrence and development of fibrosis, oxidative stress and cellular senescence are two essential factors. Oxidative stress is referred as the excessive free radicals that are produced under the stimulation of harmful factors. The excessive accumulation of oxygen free radicals and related metabolites can cause the cell to produce a variety of toxic effects. The balance between the oxidant and antioxidant systems appears to be a crucial modulator in regulating TGF-β signalling, metabolic homeostasis, and chronic inflammation, all of which are associated with the process of fibrosis. The accumulation of senescent cells caused by aging is proved as a key factor to the development of fibrosis. With the aging of the body, the increase of damaged cells and the decline in immune monitoring capabilities can reduce the clearance rate of senescent cells, and which subsequently results in the secretion of various senescence-associated secretory phenotypes (SASP), such as proinflammatory cytokines, chemokines, and metalloproteinases to accelerate the process of fibrosis.

This Special Issue welcomes original research and review articles focused on the the role of oxidative stress and cellular senescence in fibrotic diseases. We hope that the research of this Special Issue will improve the therapeutic strategies for the treatment of fibrotic diseases and provide more targets related to fibrosis under oxidative stress and senescence.

Potential topics include but are not limited to the following:

• In vivo and in vitro studies focused on the mechanisms underlying oxidative stress and cellular senescence in fibrotic diseases (including myocardial remodelling, idiopathic pulmonary fibrosis, liver fibrosis and renal fibrosis)
• Exploring novel molecular mechanisms and crosstalk between oxidative stress and cellular senescence
• Mechanisms of oxidative stress and senescence in regulating ECM secretion and the activation of pulmonary, cardiac, and liver fibroblasts
• Natural bioactive compounds regulating oxidative stress and cellular senescence in fibrotic diseases
• Molecular mechanisms of gasotransmitters in the process of fibrosis via regulating oxidative stress and cellular senescence
• Impact of atrial natriuretic peptide (ANP) secretion in oxidative stress-mediated cardiac damage and myocardial remodelling
• The role of chymase inhibitors in the development of fibrosis through modulating oxidative stress and cellular senescence
• The role of oxidative stress and cellular senescence in heart failure and myocardial remodeling during cardiac ischemia-reperfusion injury
• Oxidative stress and cellular senescence in the development of idiopathic pulmonary fibrosis (IPF)
• Regulation of oxidative stress and cellular senescence in medicine originated liver injury and fibrosis
• Novel therapeutic strategies targeting oxidative stress and cellular senescence in the treatment of fibrotic diseases