Molecular mechanisms underlying cyclophosphamide-induced ovarian injury and protective strategies

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)

Cyclophosphamide (CP) is an anti-cancer medication that also treats chronic inflammatory illnesses caused by the immune system. Although CP is widely used, it can occasionally have limited therapeutic efficacy due to its significant combined toxicities. Ovarian damage caused by CP is a major problem for patients, and premature ovarian failure (POF) is a serious side effect of CP that commonly affects female patients. Mechanistic investigations have implicated oxidative stress, inflammatory responses, and apoptosis as critical components in the etiology of CP-induced POF, although the exact process by which this ovarian toxicity occurs remains unclear. After CP causes ovarian cells to generate proinflammatory cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), nuclear factor kappa B (NF-κB) is activated. The activation of the NLRP3 inflammasome is the subsequent stage. In addition, Nrf2/HO-1 has been identified as an important signaling pathway that mitigates oxidative stress in CP-induced POF due to its anti-inflammatory and antioxidative characteristics. Moreover, several recent studies highlighted the role of α-klotho deficiency in ovarian aging. Quercetin, resveratrol, berberine, curcumin, irbesartan, mirtazapine, sildenafil, atorvastatin, donepezil, cilostazol, moxibustion, LCZ696, buspirone, levomilnacipran, melatonin, diosmin, and azilsartan

Evidence level

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

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