Table 2 The mechanism of PTEN regulating RA

Modulation of RA-FLS inflammation

Promotes the formation of arthritic aggressors and joint degeneration

Promote proliferation and migration of FLS

Promoting PTEN expression or reprogramming PTEN to induce RA-FLS, apoptosis and alleviate FLS inflammation

Blocking pathogenic Th17-type immune responses

[87]

[19]

[86]

[22]

Involved in the destruction of bone and cartilage

Indirectly involved in the regulation of angiogenic and osteoclastogenic factors, providing potential signals for the shaping of the inflammatory microenvironment

Elevated osteoclastogenic capacity of myeloid cells contributes to intensified localized bone destruction associated with increased inflammation

[99]

[100]

Indirectly induced osteoclasts enhanced NFATc1 expression, leading to a significant increase in terminal differentiation of osteoclasts in vitro

[101]

Faster osteoblast differentiation and greatly reduced apoptosis in vitro

Association with miRNAs involved in the regulation of mature osteoclast survival

Promoting mitochondrial autophagy in osteoclast precursors thereby inhibiting osteoclast formation

Decreased chondrocyte viability and type II collagen production

[104]

[105]

[106]

[107]

Involved in angiogenesis

Enhanced proliferation, migration, invasion and angiogenesis of VECs

The biological function of HUVECs in inhibiting angiogenesis is augmented by the overexpression of PTEN

PTEN overexpression reduces angiotensin II-induced damage and decreases fibrosis and inflammatory markers

Promotes maintenance of smooth muscle cell differentiation and reduces pathological vascular remodeling

Facilitated injury-induced vascular adaptation

Generalized upregulation of inflammatory and fibrosis-related genes

The establishment of an inflammatory phenotype is marked by the recruitment of progenitor cells derived from the bone marrow

[112]

[113]

[115]

[116]

[117]

[118]

[119]