Roles of ubiquitin‑specific peptidase 22 in cellular fate: From embryonic survival to tissue repair, inflammation and metabolism (Review)

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Ubiquitin‑specific peptidase 22 (USP22), a key member of the deubiquitinase family, serves pivotal roles in tumorigenesis by driving tumor proliferation, metastasis and drug resistance. In addition to its role in oncology, its versatile functions in diverse physiological and pathological contexts have been revealed. These include ensuring embryonic viability through developmental signaling regulation, promoting tissue repair and contributing to ischemia‑reperfusion injury, inflammatory responses and immune activation via cytokine and immune cell regulation. USP22 is also involved in fibrosis, metabolic homeostasis and tissue remodeling in patients with conditions such as asthma and pneumoconiosis. These multifaceted actions are mediated primarily through the deubiquitination of target proteins such as silent mating‑type information regulation 2 homologue 1 and through epigenetic mechanisms, including histone modification. The present review summarized recent advances in USP22‑mediated cell fate regulation and evaluates its therapeutic potential across diseases, underscoring promising prospects for clinical translation.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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