The myofibroblast: paradigm for a mechanically active cell.

By B. Hinz. Journal of Biomechanics, 2010

688 citations recorded by the source corpus.

Subfields: Cell Biology, Immunology and Allergy, Physiology

View Paper: https://www.semanticscholar.org/paper/5827a3d493511496fe8a4d2f05640fb2632c7462

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. Nikolaos G. Frangogiannis
2. B. Hinz
3. M. A. Pozo
4. M. Mareel
5. E. Cukierman
6. P. Keely
7. O. De Wever

In Immunology and Allergy

1. Nikolaos G. Frangogiannis
2. B. Hinz
3. E. Cukierman
4. P. Keely

In Physiology

1. Nikolaos G. Frangogiannis
2. B. Hinz
3. E. Cukierman

Citations in the corpus

• Signaling pathways in cancer-associated fibroblasts and targeted therapy for cancer (2021, background): “In these cases, activated fibroblasts secrete transforming growth factor-beta (TGF-β) and acquire a contractile phenotype via the expression of α-smooth muscle actin (α-SMA), thereby effectively closing wounds.(26) In addition, fibroblasts are also critical for the homeostasis of adjacent epithelial”
• Biomechanical remodeling of the microenvironment by stromal Caveolin-1 favors tumor invasion and metastasis (2011, background): “Fibroblast contractility is linked to SMA expression (Hinz, 2010), and SMA levels are increased in Cav1WT MEFs grown in 3D.”
• Fibroblast-specific TGF-β-Smad2/3 signaling underlies cardiac fibrosis. (2017, positive): “In addition to producing and secreting abundant ECM material, myofibroblasts acquire contractile activity through induction of genes such as Acta2 ( α -smooth muscle actin [ α SMA]), which allows these cells to physically remodel the ECM or scar after MI (7, 8).”
• Wound Healing: A Cellular Perspective. (2019, background): “Myofibroblasts are a transient cell type that deposit ECM and exhibit characteristics of contractile smooth muscle (181, 416).”
• The Pathogenesis of Cardiac Fibrosis (2013, neutral): “Myofibroblasts are phenotypically modulated fibroblasts that accumulate in sites of injury and combine ultrastructural and phenotypic characteristics of smooth muscle cells, acquired through formation of contractile stress fibers, with an extensive endoplasmic reticulum, a feature of synthetically a”
• The myofibroblast matrix: implications for tissue repair and fibrosis (2013, neutral): “For example, α-SMA-positive cells that do not form microfilament bundles are not considered myofibroblasts since they are lacking their defining contractile element [57].”
• Recent developments in myofibroblast biology: paradigms for connective tissue remodeling. (2012, background): “However, the most important defining feature of myofibroblasts is the de novo development of in vivo stress fibers and contractile force.(3,7) Several novel markers and modulators of the myofibroblast phenotype have been suggested.”
• Pathophysiology of Myocardial Infarction (2015, neutral): “Cells that form stress fibers without incorporation of α-SMA (161,162) have been identified; whether these”
• Cardiac fibrosis. (2020, background): “stressed hearts, fibroblasts undergo conversion to myofibroblasts, cells that exhibit a prominent endoplasmic reticulum (indicating a synthetically active phenotype), while expressing contractile proteins, such as asmooth muscle actin (a-SMA).(36,37) Infiltration of the heart with activated myofibro”