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Study · In vitro (cells) · 2024

3 results

Doxycycline induces mitochondrial dysfunction in aortic smooth muscle cells.

Yap C, Wanga S, Wüst RCI, van Os BW, Pijls MME, Keijzer S, van Zanten E, Koolbergen DR, Driessen AHG, Balm R, Yeung KK, de Vries CJM, Houtkooper RH, Lindeman JHN, de Waard V

Vascular pharmacology23 Jan 2024Cited by 11 (Europe PMC)

PMID38272196 (opens in a new tab)DOI10.1016/j.vph.2024.107279 (opens in a new tab)PepBankPUB-38272196
Publisher pagePubMedAsk about this study
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Summary

The antibiotic doxycycline is known to inhibit inflammation and was therefore considered as a therapeutic to prevent abdominal aortic aneurysm (AAA) growth. Yet mitochondrial dysfunction is a key-characteristic of clinical AAA disease. We hypothesize that doxycycline impairs mitochondrial function in the aorta and aortic smooth muscle cells (SMCs). Doxycycline induced mitonuclear imbalance, reduced proliferation and diminished expression of typical contractile smooth muscle cell (SMC) proteins. To understand the underlying mechanism, we studied krüppel-like factor 4 (KLF4). The expression of this transcription factor was enhanced in SMCs after doxycycline treatment. Knockdown of KLF4, however, did not affect the doxycycline-induced SMC phenotypic changes. Then we used the bioenergetics drug elamipretide (SS-31). Doxycycline-induced loss of SMC contractility markers was not rescued, but mitochondrial genes and mitochondrial connectivity improved upon elamipretide. Thus while doxycycline is anti-inflammatory, it also induces mitochondrial dysfunction in aortic SMCs and causes SMC phenotypic switching, potentially contributing to aortic aneurysm pathology. The drug elamipretide helps mitigate the harmful effects of doxycycline on mitochondrial function in aortic SMC, and may be of interest for treatment of aneurysm diseases with pre-existing mitochondrial dysfunction.
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 aortic smooth muscle cells treated with doxycycline, elamipretide did not rescue the loss of contractility markers.

    In plain wordsIn cells, elamipretide did not restore the contractility markers that doxycycline had reduced.

    Peptide
    Elamipretide (SS-31)
    Outcome
    No significant changeDoxycycline-induced loss of SMC contractility markers
    Study

    n: not reported in source

    Aortic smooth muscle cells treated with doxycycline
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Doxycycline-induced loss of SMC contractility markers was not rescued
    1 context sentence
    Summary · context
    We hypothesize that doxycycline impairs mitochondrial function in the aorta and aortic smooth muscle cells (SMCs).
  2. 02LabIn vitro (cells)Mechanism

    In aortic smooth muscle cells treated with doxycycline, elamipretide improved mitochondrial genes.

    In plain wordsIn cells, elamipretide improved mitochondrial gene expression that doxycycline had impaired.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseMitochondrial gene expression
    Study

    n: not reported in source

    Aortic smooth muscle cells treated with doxycycline
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    but mitochondrial genes and mitochondrial connectivity improved upon elamipretide.
    1 context sentence
    Summary · context
    We hypothesize that doxycycline impairs mitochondrial function in the aorta and aortic smooth muscle cells (SMCs).
  3. 03LabIn vitro (cells)Mechanism

    In aortic smooth muscle cells treated with doxycycline, elamipretide improved mitochondrial connectivity.

    In plain wordsIn cells, elamipretide improved the connectivity of mitochondria that doxycycline had impaired.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseMitochondrial connectivity
    Study

    n: not reported in source

    Aortic smooth muscle cells treated with doxycycline
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    but mitochondrial genes and mitochondrial connectivity improved upon elamipretide.
    1 context sentence
    Summary · context
    We hypothesize that doxycycline impairs mitochondrial function in the aorta and aortic smooth muscle cells (SMCs).

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

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