Association Between Rotator Cuff Tears and Calcific Tendinopathy

Louwerens, Jan K. G.; Alkaduhimi, Hassanin; Bekerom, Michel P.J. van den

doi:10.1016/j.arthro.2020.01.007

Cited by 5 publications

(6 citation statements)

References 7 publications

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“…The expression of the transcriptor factor Mkx was the highest in the Achilles enthesis. This observation goes in line with the Col1a1 expression pattern previously described since Mkx acts as a positive regulator of collagen type I expression [53]. In a similar way, the higher expression of Sox9 in the Achilles entheses samples could cause the high expression of Col2a1 in this localization, since the expression of collagen type II by chondrocytes at the enthesis is activated by the transcription factor Sox9 [54].…”

Section: Discussionsupporting

confidence: 88%

“…Although this in vivo study demonstrated the effectiveness of their construct's design in stimulating matrix heterogeneity and fibrocartilage formation, it was conducted in an ectopic, subcutaneous athymic rat model, rather than in an orthotopic, injured enthesis model. The lack of in vivo studies exclusively addressing the use of biomimetic constructs to heal injured enthesis has been acknowledged as a challenge still to overcome [3,53]. We have tried to fill in part of that gap in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…The occurrence of ectopic ossification in both the tendon and the tendon-tobone enthesis upon injury has been observed in human and animal models as an undesired effect of the failed regeneration of the native tissue structure [10,53]. Tendon ossification is associated with severe pain and an increased risk of rupture, and although it is commonly seen in clinics, it has been poorly characterized [52].…”

Section: Discussionmentioning

confidence: 99%

“…Natural polysaccharide polymers are popular alternatives used in tendon repair [52][53][54]. They are highly biocompatible, favor cell adhesion, and their biochemical cues can even exert immunomodulatory effects [55][56][57].…”

Section: Tissue Engineering For Tendon and Enthesis Repairmentioning

confidence: 99%

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Advancing tendon-to-bone enthesis repair

Peniche Silva

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Tissue Engineering For Tendon and Enthesis Repairmentioning

confidence: 99%

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Advancing tendon-to-bone enthesis repair

Peniche Silva

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“…Traumatic HO is a frequent, destructive complication caused by traumatic events, including tendon injury [33,34], burns, spinal cord injury (SCI), traumatic brain injury (TBI), and orthopedic surgery. The incidence of HO is relatively high (about 11% in TBI, 20% in SCI, 14-35% after significant elbow trauma, and 4.7% after hip arthroscopy) [16,35,36].…”

Section: Metformin Inhibits Traumatic Ho Formation In a Tenotomy Mous...mentioning

confidence: 99%

Metformin alleviates genetic and traumatic heterotopic ossification by inhibiting infiltration and mitochondrial metabolism of myeloid cells

Fan

2024

Am J Transl Res

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Objectives: Heterotopic ossification (HO), whether hereditary or traumatic, refers to the abnormal formation of bone in extraskeletal sites, often triggered by inflammation or flare-ups. Unfortunately, there are currently no effective treatments for HO. Metformin is well-known for its anti-diabetic, anti-inflammatory, anti-aging, and anticancer effects. However, its potential role in treating HO remains uncertain. Methods: Metformin was dissolved into water and given to mice. All the mice in this study were examined by microCT and myeloid cell quantification using flow cytometry. Complex activity kit was used to examine the activity of mitochondrial complexes of myeloid cells. Results: In this study, we discovered that metformin effectively inhibits genetic and traumatic HO formation and progression. Additionally, we observed a significant increase in myeloid cells in the genetic and traumatic HO mouse model compared to uninjured mice. Notably, metformin specifically reduced the infiltration of myeloid cells into the injured sites of the genetic and traumatic HO model mice. Further investigations revealed that metformin targets mitochondrial complex I and suppresses mitochondrial metabolism in myeloid cells. Conclusion: These findings suggest that metformin suppresses HO development by potentially downregulating the mitochondrial metabolism of myeloid cells, offering a promising therapeutic option for HO treatment.

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Pristimerin suppresses AIM2 inflammasome by modulating AIM2-PYCARD/ASC stability via selective autophagy to alleviate tendinopathy

Jiang,

Xie,

et al. 2023

Autophagy

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Association Between Rotator Cuff Tears and Calcific Tendinopathy

Cited by 5 publications

References 7 publications

Advancing tendon-to-bone enthesis repair

Advancing tendon-to-bone enthesis repair

Metformin alleviates genetic and traumatic heterotopic ossification by inhibiting infiltration and mitochondrial metabolism of myeloid cells

Pristimerin suppresses AIM2 inflammasome by modulating AIM2-PYCARD/ASC stability via selective autophagy to alleviate tendinopathy

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