Cited by 54Peroxisome Proliferator-Activated ReceptorsGenetics, Aging, and Longevity in Model OrganismsParaoxonase enzyme and polymorphisms

The Functions of PPARs in Aging and Longevity

Open access
Erol, Adnan·2007·PPAR Research

Abstract

Peroxisome proliferator-activated receptors (PPARs) are key regulators in various age-associated pathophysiological processes related to energy metabolism and oxidative stress. A progressive rise of oxidative stress and related inflammatory reaction appears the hallmarks of the aging process and many age-related diseases. PPARs are important redox-sensitive transcription factors and their dyregulated activations seem to be major culprits for these pathological processes. Drugs targeting PPARs activity are already in widespread clinical use; however, based on these concepts, this review highlights the understanding of the role of PPARs in aging and indicates the necessary particular attention for the potential therapeutic uses of current PPAR agonists in age-associated diseases.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1155/2007/39654

Cites

101 of 101 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • PPAR-γ, expressed in adipose tissue, enhances insulin sensitivity.

    “as PPAR-γ, expressed in adipose tissue, enhances insulin sensitivity, while PPAR-δ, predominantly found in skeletal muscle, supports oxidative metabolism and promotes mitochondrial biogenesis”

    From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [114]

    Section 6 says PPARγ is expressed primarily in adipose tissue. Section 7 says partial or minimal PPARγ activation may improve insulin sensitivity, but also reports greater insulin sensitivity in aged mice with partial PPARγ deficiency. The unqualified claim that PPARγ enhances insulin sensitivity overstates this more conditional account; page numbers are unavailable in our copy. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • Both PPAR-γ and PPAR-δ activation may prove beneficial in maintaining metabolic flexibility during aging.

    “Both PPAR-γ and PPAR-δ activation may prove beneficial in maintaining metabolic flexibility during aging”

    From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [114]

    Section 6 (page unavailable) suggests that PPAR-β/δ agonists may be useful for age-related metabolic problems. Section 7 (page unavailable) says partial or minimal PPAR-γ activation may improve insulin sensitivity in older people, but the Conclusions favor modulating or inhibiting PPAR-γ in the elderly rather than activating it generally. The claim omits that qualification, and the paper does not specifically describe the benefit as maintaining metabolic flexibility. (LLM, conf=0.87)

    Experimental — accuracy not yet measured
  • PPAR-δ, predominantly found in skeletal muscle, supports oxidative metabolism and promotes mitochondrial biogenesis.

    “as PPAR-γ, expressed in adipose tissue, enhances insulin sensitivity, while PPAR-δ, predominantly found in skeletal muscle, supports oxidative metabolism and promotes mitochondrial biogenesis”

    From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [114]

    Section 6, “PPARs and Fuel Metabolism” (page not provided), says PPARβ/δ is abundant in skeletal muscle and links it to oxidative muscle fibres and increased fatty-acid burning capacity. The passage does not say that PPARβ/δ promotes mitochondrial biogenesis. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 5

  1. [38]Chung HY Kim HJ Kim JW Yu BP The inflammation hypothesis of aging: Molecular modulation by calorie restriction Annals of the New York Academy of Sciences 2001 928 327 335 11795524
  2. [46]Jiang C Ting AT Seed B PPAR- γ agonists inhibit production of monocyte inflammatory cytokines Nature 1998 391 82 86 9422509
  3. [56]Gulick T Cresci S Caira T Moore DD Kelly DP The peroxisome proliferator-activated receptor regulates mitochondrial fatty acid oxidative enzyme gene expression Proceedings of the National Academy of Sciences of the United States of America 1994 91 11012 11016 7971999 PMC45156
  4. [65]Erol A Energy dense high-carbohydrate and low-fat diets are the reason for the epidemic of metabolic syndrome-Novel approach to etiopathogenesis of metabolic syndrome Turkish Journal of Endocrinology and Metabolism 2001 1 1 16
  5. [90]Poynter ME Daynes DA PPAR α activation modulates cellular redox status, represses NF κB signalling and reduces inflammatory cytokine production in aging The Journal of Biological Chemistry 1998 273 49 32833 32841 9830030

Cited by

Sorted by citations

Authors
Erol, A.
Affiliations
Manisa Celal Bayar University (TR)
Corresponding author
Erol, Adnan
Venue
PPAR Research
Published
2007
Volume
2007
Pages
1-10
ISSN
  • 1687-4757 (ISSN-L)
  • 1687-4765
OpenAlex
W2099290136
Cited by
54
References
101
Citations by year
2026: 3 · 2025: 4 · 2024: 4 · 2023: 2 · 2022: 5 · 2021: 7 · 2020: 5 · 2019: 3 · 2018: 3 · 2016: 1 · 2015: 1 · 2014: 1 · 2013: 1 · 2012: 3
FWCI
0.79
Type
journal article
Language
en
Open access
Locations
  • PPAR Research (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
Keywords
peroxisome proliferator-activated receptors, aging, longevity, oxidative stress, inflammation, energy metabolism, PPAR agonists, age-related diseases, redox-sensitive transcription factors

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review