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Study · In vitro (cells) · 2024

3 results

ALCAT1-mediated abnormal cardiolipin remodelling promotes mitochondrial injury in podocytes in diabetic kidney disease.

Hao Y, Fan Y, Feng J, Zhu Z, Luo Z, Hu H, Li W, Yang H, Ding G

Cell communication and signaling : CCS10 Jan 2024Cited by 34 (Europe PMC)

PMID38200543 (opens in a new tab)PMCIDPMC10777643 (opens in a new tab)DOI10.1186/s12964-023-01399-4 (opens in a new tab)PepBankPUB-38200543
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Summary

BackgroundCardiolipin (CL) plays a critical role in maintaining mitochondrial membrane integrity and overall mitochondrial homeostasis. Recent studies have suggested that mitochondrial damage resulting from abnormal cardiolipin remodelling is associated with the pathogenesis of diabetic kidney disease (DKD). Acyl-coenzyme A:lyso-cardiolipin acyltransferase-1 (ALCAT1) was confirmed to be involved in the progression of Parkinson's disease, diet-induced obesity and other ageing-related diseases by regulating pathological cardiolipin remodelling. Thus, the purpose of this investigation was to determine the role of ALCAT1-mediated CL remodelling in DKD and to explore the potential underlying mechanism.MethodsIn vivo study, the mitochondrial structure was examined by transmission electron microscopy (TEM). The colocalization of ALCAT1 and synaptopodin was evaluated by double immunolabelling. Western blotting (WB) was performed to assess ALCAT1 expression in glomeruli. Lipidomics analysis was conducted to evaluate the composition of reconstructed cardiolipins. In vitro study, the lipidomics, TEM and WB analyses were similar to those in vivo. Mitochondrial function was evaluated by measuring the mitochondrial membrane potential (MMP) and the production of ATP and ROS.ResultsHere, we showed that increased oxidized cardiolipin (ox-CL) and significant mitochondrial damage were accompanied by increased ALCAT1 expression in the glomeruli of patients with DKD. Similar results were found in db/db mouse kidneys and in cultured podocytes stimulated with high glucose (HG). ALCAT1 deficiency effectively prevented HG-induced ox-CL production and mitochondrial damage in podocytes. In contrast, ALCAT1 upregulation enhanced ox-CL levels and podocyte mitochondrial dysfunction. Moreover, treatment with the cardiolipin antioxidant SS-31 markedly inhibited mitochondrial dysfunction and cell injury, and SS-31 treatment partly reversed the damage mediated by ALCAT1 overexpression. We further found that ALCAT1 could mediate the key regulators of mitochondrial dynamics and mitophagy through the AMPK pathway.ConclusionsCollectively, our studies demonstrated that ALCAT1-mediated cardiolipin remodelling played a crucial role in DKD, which might provide new insights for DKD treatment. Video Abstract.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

3 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Mechanism

    In podocytes, the cardiolipin antioxidant SS‑31 markedly inhibited mitochondrial dysfunction.

    In plain wordsIn kidney cells, SS‑31 strongly reduced mitochondrial dysfunction.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMitochondrial dysfunction
    Study

    n: not reported in source

    Podocytes under high glucose or ALCAT1 overexpression
    Outcome group
    Mitochondrial function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    treatment with the cardiolipin antioxidant SS-31 markedly inhibited mitochondrial dysfunction and cell injury
    1 context sentence
    Summary · context
    In vitro study, the lipidomics, TEM and WB analyses were similar to those in vivo.
  2. 02LabIn vitro (cells)Efficacy outcome

    In podocytes, the cardiolipin antioxidant SS‑31 markedly inhibited cell injury.

    In plain wordsIn kidney cells, SS‑31 strongly reduced cell injury.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseCell injury
    Study

    n: not reported in source

    Podocytes under high glucose or ALCAT1 overexpression
    Outcome group
    Kidney function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    treatment with the cardiolipin antioxidant SS-31 markedly inhibited mitochondrial dysfunction and cell injury
    1 context sentence
    Summary · context
    In vitro study, the lipidomics, TEM and WB analyses were similar to those in vivo.
  3. 03LabIn vitro (cells)Mechanism

    In podocytes, SS‑31 treatment partly reversed the damage mediated by ALCAT1 overexpression.

    In plain wordsIn kidney cells, SS‑31 partly reversed damage caused by too much ALCAT1.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseDamage from ALCAT1 overexpression
    Study

    n: not reported in source

    Podocytes under high glucose or ALCAT1 overexpression
    Outcome group
    Mitochondrial function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and SS-31 treatment partly reversed the damage mediated by ALCAT1 overexpression.
    1 context sentence
    Summary · context
    In vitro study, the lipidomics, TEM and WB analyses were similar to those in vivo.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    10 Oct 2026, 08:19 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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