LONP1 and renal fibrosis: A homozygous deletion of LONP1 results in embryonic lethal, while a reduction in LONP1 expression or activity leads to abnormal accumulation of mitochondrial proteins, inhibiting cell proliferation and inducing apoptosis, potentially triggering a range of diseases including renal fibrosis, bone metabolic disorders, neuronal dysfunction, and oocyte developmental abnormalities [14–18].