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This is the first report of a multifunctional separator for potassium‐metal batteries (KMBs). Double‐coated tape‐cast microscale AlF3 on polypropylene (AlF3@PP) yields state‐of‐the‐art electrochemical performance: symmetric cells are stable after 1000 cycles (2000 h) at 0.5 mA cm−2 and 0.5 mAh cm−2, with 0.042 V overpotential. Stability is maintained at 5.0 mA cm−2 for 600 cycles (240 h), with 0.138 V overpotential. Postcycled plated surface is dendrite‐free, while stripped surface contains smooth solid electrolyte interphase (SEI). Conventional PP cells fail rapidly, with dendrites at plating, and “dead metal” and SEI clumps at stripping. Potassium hexacyanoferrate(III) cathode KMBs with AlF3@PP display enhanced capacity retention (91% at 100 cycles vs 58%). AlF3 partially reacts with K to form an artificial SEI containing KF, AlF3, and Al2O3 phases. The AlF3@PP promotes complete electrolyte wetting and enhances uptake, improves ion conductivity, and increases ion transference number. The higher of K+ transference number is ascribed to the strong interaction between AlF3 and FSI− anions, as revealed through 19F NMR. The enhancement in wetting and performance is general, being demonstrated with ester‐ and ether‐based solvents, with K‐, Na‐, or Li‐ salts, and with different commercial separators. In full batteries, AlF3 prevents Fe crossover and cycling‐induced cathode pulverization.

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Retrograde signaling is a mechanism by which mitochondrial dysfunction is communicated to the nucleus for inducing a metabolic shift essential for cell survival. Previously we showed that partial mtDNA depletion in different cell types induced mitochondrial retrograde signaling pathway (MtRS) involving Ca+2 sensitive Calcineurin (Cn) activation as an immediate upstream event of stress response. In multiple cell types, this stress signaling was shown to induce tumorigenic phenotypes in immortalized cells. In this study we show that MtRS also induces p53 expression which was abrogated by Ca2+ chelators and shRNA mediated knock down of CnAβ mRNA. Mitochondrial dysfunction induced by mitochondrial ionophore, carbonyl cyanide m-chlorophenyl hydrazone (CCCP) and other respiratory inhibitors, which perturb the transmembrane potential, were equally efficient in inducing the expression of p53 and downregulation of MDM2. Stress-induced p53 physically interacted with HIF-1α and attenuated the latter’s binding to promoter DNA motifs. Additionally, p53 promoted ubiquitination and degradation of HIF-1α in partial mtDNA depleted cells. The mtDNA depleted cells, with inhibited HIF-1α, showed upregulation of glycolytic pathway genes, glucose transporter 1–4 (Glut1–4), phosphoglycerate kinase 1 (PGK1) and Glucokinase (GSK) but not of prolyl hydroxylase (PHD) isoforms. For the first time we show that p53 is induced as part of MtRS and it renders HIF-1α inactive by physical interaction. In this respect our results show that MtRS induces tumor growth independent of HIF-1α pathway.