Background
Maladaptive tissue remodeling and fibrosis are a typical response to injury which leads to distorted architecture, pathologic signaling and ultimately organ dysfunction. Tissue fibrosis has remained the main pathophysiological endpoint outcome leading to organ failure causing severe morbidity worldwide. Cardiovascular diseases (CVD) are a major contributor towards global mortality. Clinically, patients suffering from CVDs are often attributed with renal and pulmonary complexities. Renal and pulmonary fibrosis are also independent risk factors for heart failure. A histological hallmark of many of these end-stage pathologies is tissue fibrosis, characterized by an excessive accumulation of extracellular matrix (ECM) molecules and de-regulation of ECM modulating enzymes. The cause consequence relation between this fibrotic remodeling and patient’s outcome remains unclear – and likely depends on the type of tissue insult – yet, renal and pulmonary fibrosis are independent risk factors for heart failure patients. The degree of tissue fibrosis, comorbidities and standard of care therapies often vary among patients and there are limited effective anti-fibrotic therapies clinically approved, most of them with unclear biological mechanisms of action. Therefore, effective, safe and well-tolerated pharmacological strategies that halt fibrotic remodeling of tissues is an area of unmet but high clinical need. The challenges are to prospectively define patient populations that benefit from anti-fibrotic therapies and gain a deeper mechanistic understanding of pro-fibrotic signaling mechanisms. These molecular mechanistic understandings eventually would lay the foundation for developing next-generation therapeutics to tackle pathological fibrosis in a spatio-temporal manner.
Goal
The goal of this Research Topic is to generate a holistic overview and showcase the mechanistic understanding for pan-tissue fibrosis. Significant efforts have been undertaken and ongoing to understand cardiac fibrosis mediated heart failure. Although, systemic circulation connects different organ systems in human body, the pan-understanding of organ crosstalks contributing towards cardiac fibrosis mediated heart failure is poorly understood. In this collection, we intend to put forward a concerted effort in understanding the renal and pulmonary tissue injury mediated cardiac fibrosis pathways and mechanisms. Further, understanding the tissue-specific extra-cellular matrix remodeling during fibrosis is of special interest. The ECM architecture of different organs is diverse in nature. Thus, research articles addressing the signaling mechanisms leading to ECM remodeling during fibrosis development and progression will shed important insights in understanding the plethora of pathological diversity. Further, it would lay the foundation to understand the available potential therapeutic interventions that may be applied in managing pathology specific tissue-fibrosis.
Scope and information for Authors
In this Research Topic, the authors are encouraged to submit comprehensive reviews, original research articles, cellular signaling based studies, OMICS based studies pertaining to tissue fibrosis, animal model based mechanistic understandings, articles describing any advanced mechanisms for understanding fibrosis. A range of article types are accepted addressing, but not limited to, the following:
• Fibrosis: friend (tissue healing) or foe (fibrosis leading to organ failure)
• Fibroblast activation mechanism in pan-tissue (Heart, Lungs, Kidney) fibrosis.
• Cardiac fibrosis mechanisms: Heart failure with preserved (HFpEF) and reduced ejection (HFrEF)
• Fibroblast-immune cell interactions leading to ECM remodeling
• Mechanistic understanding of Cardiorenal or cardiopulmonary fibrosis
• Mechanisms of therapeutic targets and interventions
• Role of collagens in ECM remodeling during fibrosis
Dr. Saraswati serves as a Chief Scientific Officer at Eluciderm Inc. All other Topic Editors declare no competing interests.
Background
Maladaptive tissue remodeling and fibrosis are a typical response to injury which leads to distorted architecture, pathologic signaling and ultimately organ dysfunction. Tissue fibrosis has remained the main pathophysiological endpoint outcome leading to organ failure causing severe morbidity worldwide. Cardiovascular diseases (CVD) are a major contributor towards global mortality. Clinically, patients suffering from CVDs are often attributed with renal and pulmonary complexities. Renal and pulmonary fibrosis are also independent risk factors for heart failure. A histological hallmark of many of these end-stage pathologies is tissue fibrosis, characterized by an excessive accumulation of extracellular matrix (ECM) molecules and de-regulation of ECM modulating enzymes. The cause consequence relation between this fibrotic remodeling and patient’s outcome remains unclear – and likely depends on the type of tissue insult – yet, renal and pulmonary fibrosis are independent risk factors for heart failure patients. The degree of tissue fibrosis, comorbidities and standard of care therapies often vary among patients and there are limited effective anti-fibrotic therapies clinically approved, most of them with unclear biological mechanisms of action. Therefore, effective, safe and well-tolerated pharmacological strategies that halt fibrotic remodeling of tissues is an area of unmet but high clinical need. The challenges are to prospectively define patient populations that benefit from anti-fibrotic therapies and gain a deeper mechanistic understanding of pro-fibrotic signaling mechanisms. These molecular mechanistic understandings eventually would lay the foundation for developing next-generation therapeutics to tackle pathological fibrosis in a spatio-temporal manner.
Goal
The goal of this Research Topic is to generate a holistic overview and showcase the mechanistic understanding for pan-tissue fibrosis. Significant efforts have been undertaken and ongoing to understand cardiac fibrosis mediated heart failure. Although, systemic circulation connects different organ systems in human body, the pan-understanding of organ crosstalks contributing towards cardiac fibrosis mediated heart failure is poorly understood. In this collection, we intend to put forward a concerted effort in understanding the renal and pulmonary tissue injury mediated cardiac fibrosis pathways and mechanisms. Further, understanding the tissue-specific extra-cellular matrix remodeling during fibrosis is of special interest. The ECM architecture of different organs is diverse in nature. Thus, research articles addressing the signaling mechanisms leading to ECM remodeling during fibrosis development and progression will shed important insights in understanding the plethora of pathological diversity. Further, it would lay the foundation to understand the available potential therapeutic interventions that may be applied in managing pathology specific tissue-fibrosis.
Scope and information for Authors
In this Research Topic, the authors are encouraged to submit comprehensive reviews, original research articles, cellular signaling based studies, OMICS based studies pertaining to tissue fibrosis, animal model based mechanistic understandings, articles describing any advanced mechanisms for understanding fibrosis. A range of article types are accepted addressing, but not limited to, the following:
• Fibrosis: friend (tissue healing) or foe (fibrosis leading to organ failure)
• Fibroblast activation mechanism in pan-tissue (Heart, Lungs, Kidney) fibrosis.
• Cardiac fibrosis mechanisms: Heart failure with preserved (HFpEF) and reduced ejection (HFrEF)
• Fibroblast-immune cell interactions leading to ECM remodeling
• Mechanistic understanding of Cardiorenal or cardiopulmonary fibrosis
• Mechanisms of therapeutic targets and interventions
• Role of collagens in ECM remodeling during fibrosis
Dr. Saraswati serves as a Chief Scientific Officer at Eluciderm Inc. All other Topic Editors declare no competing interests.
