# PERM1--An Emerging Transcriptional Regulator of Mitochondrial Biogenesis: A Systematic Review
## 3 Results

Table 2: Studies examining PERM1 in the cardiac muscle. \begin{table}
\begin{tabular}{c c c} \hline \hline
**Author** & **Model/Intervention** & **Key Findings** \\ \hline \multirow{6}{*}{[25]} & Isolated mitochondria from mouse hearts & \(\bullet\) & PERM1 is co-located with the mitochondrial marker TOM20, indicating that PERM1 is located in the outer mitochondrial membrane. \\ \cline{2-3}  & Hearts of mice & \(\bullet\) & PERM1 protein levels increase during early heart development after birth. \\  & & \(\bullet\) & PERM1 is phosphorylated by CK2 kinase. \\ \cline{2-3}  & PERM1 knockdown mice & \(\bullet\) & Reduced protein expression of LPIN1—modulator of lipid homeostasis—in the mitochondrial fraction of the heart tissue. \\ \cline{2-3}  & Human & \(\bullet\) & PERM1 is more predominant in the outer mitochondrial membrane of the human heart tissue. \\ \hline \multirow{6}{*}{[33]} & & \(\bullet\) & In PERM1-deficient hearts, mitochondrial cristate demonstrate reduced density and increased disorganization, reduced OxPhos protein levels, and increased glycolysis. \\  & Mice & \(\bullet\) & In mouse hearts under pressure overload, PERM1-induced transcriptional regulation of ERR target genes is reduced. \\  & & \(\bullet\) & Hearts from PERM knockdown mice show increased accumulation of glycolytic and polyoluminescent intermediates, enhanced glycerolipid biosynthesis, and reduced levels of free fatty acids and monoglycer. \\ \cline{2-3}  & Cardiomyocytes & \(\bullet\) & PERM1 physically interacts with ERR\(\alpha\), ANKRD1, BAC6, KANK2, and TIFI\(\beta\). \\ \hline \multirow{6}{*}{[34]} & Cardiomyocytes & \(\bullet\) & PERM1 knockdown in cardiomyocytes impairs PPAR\(\alpha\)-mediated transcription, while PGC-1\(\alpha\) knockdown inhibits PERM1-induced transcriptional activation via PPRE. \\ \cline{2-3}  & Mice & \(\bullet\) & PERM1 knockdown mouse hearts experience downregulation of several genes implicated in fatty acid metabolism (_CPT1\(\beta\), CPT2, ACADM, LCAD_, and VLCAD) and carbohydrate metabolism (_SLC2A1_, _SLC2A4_, _HK1_, _HK2_, _PDK4_, and ALDOA). \\  & & \(\bullet\) & The transcription of genes implicated in fatty acid metabolism in mouse hearts is mediated by PERM1 interactions with PPAR\(\alpha\) and PGC-1\(\alpha\). \\ \hline \multirow{6}{*}{[35]} & & Mice & \(\bullet\) & PERM1 binds to lamin A protein. \\ \cline{2-3}  & & \(\bullet\) & Pressure overload in hearts overexpressing PERM1 causes upregulated levels of MICOS and OxPhos proteins and increased mitochondrial DNA copy number. \\  & & \(\bullet\) & PERM1 binds to the Mic60 protein in heart lysates. \\  & & \(\bullet\) & In cardiomyocyteytes. \\ \cline{2-3}  & Mice & \(\bullet\) & Decreased Mic60 expression reduces MICOS and OxPhos protein levels. \\  & & \(\bullet\) & PERM1 overexpression increases Mic60 and Mic10 protein levels and maintains the levels of MICOS proteins, when Mic60 shRNA is induced. \\  & & \(\bullet\) & Mic60 loss-of-function decreases the maximal oxygen consumption rate even when PERM1 is overexpressed. \\ \hline \hline \end{tabular}
\end{table} 
Table 2: _Cont._