Tissue remodeling

Tissue remodeling is the reorganization or renovation of existing tissues. Tissue remodeling can be either physiological or pathological. The process can either change the characteristics of a tissue such as in blood vessel remodeling, or result in the dynamic equilibrium of a tissue such as in bone remodeling. Macrophages repair wounds and remodel tissue by producing extracellular matrix and proteases to modify that specific matrix.[1]

A myocardial infarction induces tissue remodeling of the heart in a three-phase process: inflammation, proliferation, and maturation. Inflammation is characterized by massive necrosis in the infarcted area. Inflammatory cells clear the dead cells. In the proliferation phase, inflammatory cells die by apoptosis, being replaced by myofibroblasts which produce large amounts of collagen. In the maturation phase, myofibroblast numbers are reduced by apoptosis, allowing for infiltration by endothelial cells (for blood vessels) and cardiomyocytes (heart tissue cells). Usually, however, much of the tissue remodeling is pathological, resulting in a large amount of fibrous tissue.[2] By contrast, aerobic exercise can produce beneficial cardiac tissue remodeling in those suffering from left ventricular hypertrophy.[3]

Programmed cellular senescence contributes to beneficial tissue remodeling during embryonic development of the fetus.[4]

In a brain stroke the penumbra area surrounding the ischemic event initially undergoes a damaging remodeling, but later transitions to a tissue remodeling characterized by repair.[5]

Vascular remodeling refers to a compensatory change in blood vessel walls due to plaque growth. Vascular expansion is called positive remodeling, whereas vascular constriction is called negative remodeling.[6]

Tissue remodeling occurs in adipose tissue with increased body fat.[7] In obese subjects, this remodeling is often pathological, characterized by excessive inflammation and fibrosis.[8]

See also

  • Collagen hybridizing peptide, a molecular marker to directly image tissue remodeling

References

  1. ↑ Lee BC, Lee J (2014). "Cellular and molecular players in adipose tissue inflammation in the development of obesity-induced insulin resistance". Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1842 (3): 446–462. doi:10.1016/j.bbadis.2013.05.017. PMC 3800253. PMID 23707515.
  2. ↑ Talman V, Ruskoaho H (2016). "Cardiac fibrosis in myocardial infarction-from repair and remodeling to regeneration". Cell and Tissue Research. 365 (3): 563–581. doi:10.1007/s00441-016-2431-9. PMC 5010608. PMID 27324127.
  3. ↑ Fernandes T, Baraúna VG, Negrão CE, Phillips MI, Oliveira EM (2015). "Aerobic exercise training promotes physiological cardiac remodeling involving a set of microRNAs". American Journal of Physiology. Heart and Circulatory Physiology. 309 (4): H543–H552. doi:10.1152/ajpheart.00899.2014. PMC 4537939. PMID 26071549.
  4. ↑ Khosla S, Farr JN, Tchkonia T, Kirkland JL (2020). "The role of cellular senescence in ageing and endocrine disease". Nature Reviews Endocrinology. 16 (5): 263–275. doi:10.1038/s41574-020-0335-y. PMC 7227781. PMID 32161396.
  5. ↑ Lo EH (2008). "A new penumbra: transitioning from injury into repair after stroke". Nature Medicine. 14 (5): 497–500. doi:10.1038/nm1735. PMID 18463660. S2CID 205385488.
  6. ↑ Lee CS, Seo YH, Yang DJ, Kim KH, Park HW, Yuk HB, Lee MS, Kim WH, Kwon TG, Bae JH (2012). "Positive Vascular Remodeling in Culprit Coronary Lesion is Associated With Plaque Composition: An Intravascular Ultrasound-Virtual Histology Study". Korean Circulation Journal. 42 (11): 747–752. doi:10.4070/kcj.2012.42.11.747. PMC 3518708. PMID 23236326.
  7. ↑ Itoh M, Suganami T, Hachiya R, Ogawa Y (2011). "Adipose tissue remodeling as homeostatic inflammation". International Journal of Inflammation. 2011: 720926. doi:10.4061/2011/720926. PMC 3132651. PMID 21755030.
  8. ↑ Choe SS, Huh JY, Hwang IJ, Kim JI, Kim JB (2016). "Adipose Tissue Remodeling: Its Role in Energy Metabolism and Metabolic Disorder". Frontiers in Endocrinology. 7: 30. doi:10.3389/fendo.2016.00030. PMC 4829583. PMID 27148161.


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