TABLE 1.
Impact of global Mϕ depletion on AKI and its outcomes.
| AKI model | Depletion method | Outcomes |
| Impact of global Mϕ depletion on AKI and its outcomes: beneficial | ||
| UUO | Clodronate (before and at day 2 and 4 of UUO) | Reduced tubular apoptosis and fibrosis (Kitamoto et al., 2009) |
| UUO | Small molecule CSF-1R inhibitor (Fms-I; starting before UUO and 2× daily) | Reduced tubular apoptosis; no change in fibrosis (Ma et al., 2009) |
| UUO | CSF1 deficiency (knockout) | Reduced tubular apoptosis (Lenda et al., 2003) |
| Unilateral IRI | IL-34 deficiency (knockout) | Improved kidney function; reduced fibrosis (Baek et al., 2015) |
| Hypertension (high dose angiotensin II injections) | Clodronate (before and every 3 days till the end of the experiments) | Reduced renal injury and fibrosis; lowered blood pressure (Huang et al., 2018) |
| UUO | Clodronate (every 2 days starting day 1 before UUO) | Reduced fibrosis (Liu et al., 2018) |
| Impact of global Mϕ depletion on AKI and its outcomes: harmful | ||
| DT-induced depletion of Ggt1-expressing proximal tubules | Clodronate or DT-induced depletion of CD11c+ cells | Reduced survival (Zhang et al., 2012) |
| DT-induced depletion of Ggt1-expressing proximal tubules or unilateral IRI | Proximal tubule-specific CSF1 deficiency (conditional knockout) | Delayed functional + structural recovery from AKI; increased fibrosis (Wang et al., 2015) |