Fibrosis is necessary to repair damaged tissues and organs. However, excessive fibrosis leads to abnormal remodeling and progressive dysfunction of multiple organs, including the heart, kidney, pulmonary, liver, etc. In addition, stress response and injury (such as ischemia, metabolism abnormality, chemotherapy, radiotherapy, alcohol, autoimmune diseases, and so on) can cause organ fibrosis. The pathogenesis and mechanisms involve an activated renin-angiotensin-aldosterone system (RAAS), oxidative stress, maladaptive inflammation, lipotoxicity, mitochondrial disorders, impaired autophagy, apoptosis, and various signaling pathways, such as membrane-tethered disintegrin and metalloproteases (ADAMs), FoxO, AMPK, and Ca2+ signaling.
According to the different pathogenesis and mechanisms of fibrosis, the therapeutic strategies might differ in duration and molecular targets. For example, Myofibroblast differentiation represents one critical therapeutic target because of its essential role in collagen production. However, the lack of specific markers makes the field of fibrosis particularly challenging to explore. Moreover, it is urgent to screen new circulating biomarkers and imaging methods to examine the extent of organ fibrosis and evaluate treatment efficiency.
For this Research Topic, we welcome researchers to submit original research articles, pooled analyses, and review articles that will contribute to the field of organ fibrosis. We welcome the basic and clinical studies focusing on the etiology, pathophysiology, measurements, and fibrosis therapy.
This Research Topic is interested in the following research fields (but not limited):
• Preclinical studies to explore the mechanisms of fibrosis, including disordered RAAS and autophagy, as well as impaired ADAMs, FoxO, AMPK, and Ca2+ signaling, in cardiomyocytes and other cells
• Circulating biomarkers of organ fibrosis
• New imaging methods to evaluate organ fibrosis
• Organ fibrosis induced by ischemia, metabolism abnormality, chemotherapy, radiotherapy, alcohol, or autoimmune diseases
• Role of myofibroblasts in physiology and pathophysiology of the heart, kidney, pulmonary, liver, and so on
• New therapeutic strategies to prevent, alleviate or reverse fibrosis, remodeling and dysfunction of the heart, kidney, pulmonary, liver, and so on
Fibrosis is necessary to repair damaged tissues and organs. However, excessive fibrosis leads to abnormal remodeling and progressive dysfunction of multiple organs, including the heart, kidney, pulmonary, liver, etc. In addition, stress response and injury (such as ischemia, metabolism abnormality, chemotherapy, radiotherapy, alcohol, autoimmune diseases, and so on) can cause organ fibrosis. The pathogenesis and mechanisms involve an activated renin-angiotensin-aldosterone system (RAAS), oxidative stress, maladaptive inflammation, lipotoxicity, mitochondrial disorders, impaired autophagy, apoptosis, and various signaling pathways, such as membrane-tethered disintegrin and metalloproteases (ADAMs), FoxO, AMPK, and Ca2+ signaling.
According to the different pathogenesis and mechanisms of fibrosis, the therapeutic strategies might differ in duration and molecular targets. For example, Myofibroblast differentiation represents one critical therapeutic target because of its essential role in collagen production. However, the lack of specific markers makes the field of fibrosis particularly challenging to explore. Moreover, it is urgent to screen new circulating biomarkers and imaging methods to examine the extent of organ fibrosis and evaluate treatment efficiency.
For this Research Topic, we welcome researchers to submit original research articles, pooled analyses, and review articles that will contribute to the field of organ fibrosis. We welcome the basic and clinical studies focusing on the etiology, pathophysiology, measurements, and fibrosis therapy.
This Research Topic is interested in the following research fields (but not limited):
• Preclinical studies to explore the mechanisms of fibrosis, including disordered RAAS and autophagy, as well as impaired ADAMs, FoxO, AMPK, and Ca2+ signaling, in cardiomyocytes and other cells
• Circulating biomarkers of organ fibrosis
• New imaging methods to evaluate organ fibrosis
• Organ fibrosis induced by ischemia, metabolism abnormality, chemotherapy, radiotherapy, alcohol, or autoimmune diseases
• Role of myofibroblasts in physiology and pathophysiology of the heart, kidney, pulmonary, liver, and so on
• New therapeutic strategies to prevent, alleviate or reverse fibrosis, remodeling and dysfunction of the heart, kidney, pulmonary, liver, and so on
