porhon, it could well be as you say, but tell me how did you come to speculate that. My understanding of cytostorms is weak but I did find this article below telling that Mdivi-1 attenuates acute lung injury and calms down pro-inflammatory cytokines mitochondrial fission. As you may remember PBT434 is chemically very similar to Mdivi-1 ( both quinazolinones ) and in experiments, both of these are working in similar ways.

IMO it would be a good thing if Sinclair would be investigating if PBT434 could calm down the lung problem in the COVID-19 cases.

Here is this paper

Pulm Pharmacol Ther

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. 2020 Apr 3;62:101918.

doi: 10.1016/j.pupt.2020.101918. Online ahead of print.

Mdivi-1 Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Inhibiting MAPKs, Oxidative Stress and Apoptosis

Songyun Deng ¹ , Lina Zhang ² , Yunan Mo ³ , Yan Huang ⁴ , Wenchao Li ⁵ , Qianyi Peng ⁶ , Li Huang ⁷ , Yuhang Ai ⁸

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• PMID: 32251714
• DOI: 10.1016/j.pupt.2020.101918

Abstract

Sepsis is among the most devastating events in intensive care units. As a complication of sepsis, acute lung injury (ALI) is common and highly associated with poor outcome. The present study demonstrated that abnormal mitochondrial dynamics play a pivotal role in lipopolysaccharide (LPS)-induced ALI. Inhibiting the mitochondrial fission with the specific inhibitor-1 (Mdivi-1) ameliorated ALI as assessed by hematoxylin and eosin (H&E) staining and wet/dry ratio. Furthermore, Mdivi-1 reduced mitogen-activated protein kinases (MAPKs) activation, oxidative stress and apoptosis in the lungs. Plasma pro-inflammation cytokines were also reduced significantly in Mdivi-1-treated mice. In vitro study revealed that Mdivi-1 protected the macrophages from LPS-induced MAPKs activation, oxidative stress and cell apoptosis. Mdivi-1 also inhibited the release of pro-inflammatory cytokines. Morphological analysis showed that Mdivi-1 rescued the macrophages from LPS-induced mitochondrial fragmentation. Moreover, LPS treatment induced significant phosphorylation of Drp1 at Ser616, dephosphorylation at Ser637 and translocation of Drp1 from the cytoplasm to mitochondria, while Mdivi-1 inhibited those effects. Thus, modification of fission to rebuild mitochondrial homeostasis may offer an innovative opportunity for developing therapeutic strategies against ALI.