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Last update 08 May 2025

SPARCL1

Last update 08 May 2025

Basic Info

Synonyms

Hevin, High endothelial venule protein, MAST 9

+ [4]

Introduction-

Drugs associated with SPARCL1

CN116036236

Patent Mining

Target

SPARCL1

Mechanism-

Active Org.

Southeast University

Originator Org.

Southeast University

Active Indication

Neurologic Manifestations

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with SPARCL1

100 Translational Medicine associated with SPARCL1

0 Patents (Medical) associated with SPARCL1

276

Literatures (Medical) associated with SPARCL1

01 Apr 2025·Molecular Therapy

AAV-Sparcl1 promotes hair cell regeneration by increasing supporting cell plasticity

Article

Author: Li, Nianci ; Sun, Qiuhan ; Zhou, Yinyi ; Zhang, Liyan ; Qi, Jieyu ; Zhang, Ziyu ; Tan, Fangzhi ; Ding, Xiaoqiong ; Qian, Xiaoyun ; Wang, Man ; Ye, Fanglei ; Chai, Renjie ; Lu, Yicheng

Sensorineural hearing deficiency caused by hair cell damage represents a prevalent sensory deficit disorder. In mammals, age-related reduction in plasticity of inner ear supporting cells (recognized as hair cell precursors) compromises their trans-differentiation capacity, resulting in impaired spontaneous hair cell regeneration post-injury. Therapeutic reprogramming of supporting cells to functionally replace damaged hair cells has emerged as a promising strategy for sensorineural hearing loss treatment. In this study, we demonstrate that the secretory protein Sparcl1 enhances supporting cell reprogramming and hair cell regeneration in both in vitro and in vivo models. Through the adeno-associated virus (AAV)-mediated overexpression system, we successfully achieved in vivo expansion of inner ear organoids accompanied by hair cell differentiation. RNA-seq analysis revealed that Sparcl1 overexpression stimulates supporting cell proliferation via follistatin (Fst) activation and extracellular matrix (ECM) remodeling. Notably, both AAV-ie-Sparcl1 delivery and recombinant Sparcl1 protein administration effectively induced supporting cell differentiation into hair cells in vivo. Collectively, our findings establish Sparcl1 as a potent positive regulator of hair cell regeneration and elucidate mechanisms by which secretory proteins regulate supporting cell plasticity.

01 Apr 2025·ESC Heart Failure

SPARCL1 and NT‐proBNP as biomarkers of right ventricular‐to‐pulmonary artery uncoupling in pulmonary hypertension

Article

Author: Sossalla, Samuel ; Gall, Henning ; Richter, Manuel J. ; van Wickern, Paulina ; Liebetrau, Christoph ; Yogeswaran, Athiththan ; Nef, Holger ; Keranov, Stanislav ; Ghofrani, Ardeschir ; Dörr, Oliver ; Tello, Khodr ; Hamm, Christian ; Bauer, Pascal ; Seeger, Werner ; Troidl, Christian ; Voss, Sandra

AbstractAimsSPARCL1 was recently identified as a biomarker of right ventricular (RV) maladaptation in patients with pulmonary hypertension (PH), and N‐terminal pro‐brain natriuretic protein (NT‐proBNP) is an established biomarker of RV failure in PH. The present study investigated whether NT‐proBNP and SPARCL1 concentrations are associated with load‐independent parameters of RV function and RV‐to‐pulmonary artery (RV–PA) coupling as measured using invasive pressure–volume (PV) loops in the RV.MethodsSPARCL1 and NT‐proBNP were measured in the plasma of patients with idiopathic pulmonary artery hypertension (IPAH, n = 73). Participants without LV or RV abnormalities served as controls (n = 28). All patients underwent echocardiography and right heart catheterization with invasive PV loop measurements.ResultsOur cohort had more females with IPAH than the control group (64% vs. 35%; P = 0.01) and was older [69 (interquartile range, IQR 57–76) vs. 51 (IQR 35–62) years; P < 0.001]. SPARCL1 and NT‐proBNP levels were significantly higher in patients with IPAH as compared with controls (P < 0.0001). Patients with IPAH and maladaptive RV remodelling had higher SPARCL1 and NT‐proBNP concentrations than those with adaptive RV remodelling (P < 0.01). Both SPARCL1 and NT‐proBNP were good predictors of maladaptive RV remodelling in receiver operating characteristic analysis [area under the curve (AUC) (AUCSPARCL1 = 0.75, AUCNT‐proBNP = 0.72, P = 0.36 for AUCSPARCL1 vs. AUCNT‐proBNP]. The combined predictive value of SPARCL1 and NT‐proBNP (AUC 0.78, P < 0.001) for maladaptive RV was numerically higher than that of either SPARCL1 or NT‐proBNP alone (P = 0.16 for AUCSPARCL1 + NT‐proBNP vs. AUCNT‐proBNP and P = 0.18 for AUCSPARCL1 + NT‐proBNP vs. AUCSPARC1). SPARCL1 showed numerically a tendency for a better predictive power than NT‐proBNP for parameters of early maladaptive RV remodelling such as RV ejection fraction < 50% (AUCSPARCL1 = 0.77, AUCNT‐proBNP = 0.67, P = 0.06 for AUCSPARCL1 vs. AUCNT‐proBNP), RV end‐diastolic diameter > 42 mm (AUCSPARCL1 = 0.72, AUCNT‐proBNP = 0.65, P = 0.19 for AUCSPARCL1 vs. AUCNT‐proBNP) and RV end‐systolic volume index RVESVI > 31 mL/m2 (AUCSPARCL1 = 0.78, AUCNT‐proBNP = 0.71, PP = 0.10 for AUCSPARCL1 vs. AUCNT‐proBNP).ConclusionsSPARCL1 and NT‐proBNP are good predictors of maladaptive RV remodelling and RV–PA uncoupling in IPAH patients. SPARCL1 may be a better predictor of early maladaptive RV remodelling than NT‐proBNP.

01 Apr 2025·Stem Cell Reports

The lung microvasculature promotes alveolar type 2 cell differentiation via secreted SPARCL1

Article

Author: Cleaver, Ondine ; Kim, Hyun-Taek ; Lautenschläger, Till ; Günther, Stefan ; Alayoubi, Yousef ; Looso, Mario ; Stainier, Didier Y R ; Panza, Paolo ; Piesker, Janett

Lung endothelial cells (ECs) and pericytes are closely juxtaposed with the respiratory epithelium before birth and thus may have instructive roles during development. To test this hypothesis, we screened EC-secreted proteins for their ability to alter cell differentiation in alveolar organoids. We identified secreted protein acidic and rich in cysteine-like protein 1 (SPARCL1) as an extracellular matrix molecule that can promote alveolar type 2 (AT2) cell differentiation in vitro. SPARCL1-treated organoids display lysozyme upregulation and a doubling in the number of AT2 cells at the expense of intermediate progenitors. SPARCL1 also induces the upregulation of nuclear factor κB (NF-κB) target genes, and suppression of NF-κB activation in lung organoids blocked SPARCL1 effects. NF-κB activation by lipopolysaccharide (LPS) was sufficient to induce AT2 cell differentiation; however, pharmacological inhibition of the pathway alone did not prevent it. These data support a role for SPARCL1 and NF-κB in alveolar cell differentiation and suggest a potential value in targeting this signaling axis to promote alveolar maturation and regeneration.

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