Evidence map›Paper›PMID 40875440›Full record

ArticleThe Journal of clinical investigation2025

A smooth muscle cell lncRNA controls angiogenesis in chronic limb-threatening ischemia through miR-143-3p/HHIP signaling.

Ming Zhai, Anurag Jamaiyar, Jun Qian, Winona W Wu, Emre Bektik, Vinay Randhawa, Camila Vaz, Arvind K Pandey, Akm Khyrul Wara, Madhur Sachan and 6 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. TheNon-coding RNA · 2026
    Article
  2. Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Ming ZhaiCardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Anurag JamaiyarCardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Jun QianCardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Winona W WuCardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Emre BektikCardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Vinay RandhawaCardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Camila VazCardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Arvind K PandeyCardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Akm Khyrul WaraCardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Madhur SachanCardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Yi HuCardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Jéssica L GarciaCardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Claire E AlfordCardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Terence E RyanDepartment of Applied Physiology and Kinesiology, University of Florida, Gainesville, Florida, USA.
Wenhui PengDepartment of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Mark W FeinbergCardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Funding

STRUCTURE-FUNCTION RELATIONSHIPS IN THE ALIMENTARY TRACTP30DK034854 · NIDDK · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WAYNE I LENCER · 1986 to 2026
$32.4M
MiR-181b, endothelial cells, and vascular inflammationR01HL115141 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI FEINBERG, MARK W · 2012 to 2024
$6.8M
miR-615, AKT/eNOS signaling, and angiogenesisR01HL148207 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI FEINBERG, MARK W · 2020 to 2023
$2.6M
LncRNA SNHG12, vascular senescence, and atherosclerosisR01HL148355 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI FEINBERG, MARK W · 2020 to 2023
$2.5M
KLF10, CD4+ T cells, and transplant arteriopathyR01HL134849 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI FEINBERG, MARK W · 2017 to 2020
$1.7M
LncRNA MAARS, macrophage apoptosis, and atherosclerosisR01HL153356 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI FEINBERG, MARK W · 2020 to 2023
$1.7M
LncRNA MERRICAL, macrophage chemotaxis, and diabetes-associated atherosclerosisR01HL171239 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI FEINBERG, MARK W · 2024 to 2025
$1.3M
miR-130b, angiogenesis, and diabetic critical limb ischemiaR01HL167905 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI FEINBERG, MARK W · 2024 to 2025
$1.3M
NHLBI NIH HHS R01 HL115141NHLBI NIH HHS R01 HL134849NHLBI NIH HHS R01 HL148207NHLBI NIH HHS R01 HL148355NHLBI NIH HHS R01 HL153356NHLBI NIH HHS R01 HL167905NHLBI NIH HHS R01 HL171239NIDDK NIH HHS P30 DK034854
6 · The paper itself

Abstract

Peripheral artery disease (PAD) often advances to chronic limb-threatening ischemia (CLTI), resulting in severe complications such as limb amputation. Despite the potential of therapeutic angiogenesis, the mechanisms of cell-cell communication and transcriptional changes driving PAD are not fully understood. Profiling long noncoding RNAs (lncRNAs) from gastrocnemius muscles of participants with or without CLTI revealed that a vascular smooth muscle cell-enriched (SMC-enriched) lncRNA, CARMN, was reduced with CLTI. This study explored how a SMC lncRNA-miRNA signaling axis regulates angiogenesis in limb ischemia. CARMN-KO mice exhibited reduced capillary density and impaired blood flow recovery and tissue necrosis following limb ischemia. We found that CARMN-KO SMC supernatants inhibited endothelial cell (EC) proliferation, spheroid sprouting, and network formation. RNA-seq identified downregulation of the Hedgehog signaling pathway in CARMN-KO models and revealed that CARMN regulates this pathway through its downstream miRNA, miR-143-3p, which targets Hedgehog-interacting protein (HHIP), an antagonist of Hedgehog signaling. Delivery of HHIP-specific siRNA or miR-143-3p mimics rescued EC angiogenic defects and improved blood flow recovery in both CARMN-KO and WT mice. These findings underscore the critical role of CARMN in modulating angiogenesis through the miR-143-3p-HHIP-Hedgehog signaling axis, providing insights into SMC-EC interactions and potential therapeutic strategies for CLTI.

Indexed as

Chronic Limb-Threatening IschemiaIschemiaMicroRNAsMyocytes, Smooth MuscleNeovascularization, PhysiologicRNA, Long NoncodingSignal TransductionAngiogenesisAnimalsHumansMaleMiceMice, KnockoutMicroRNAsMIRN143 microRNA, humanMIRN143 microRNA, mouseRNA, Long NoncodingAngiogenesisCardiovascular diseaseEndothelial cellsNoncoding RNAsVascular biology

Identifiers

PMID40875440
PMCPMC12520679

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.